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Seminal plasma contains a heterogeneous population of extracellular vesicles (sEVs) that remains poorly characterized. This study aimed to characterize the lipidomic profile of two subsets of differently sized sEVs, small (S-) and large (L-), isolated from porcine seminal plasma by size-exclusion chromatography and characterized by an orthogonal approach. High-performance liquid chromatography–high-resolution mass spectrometry was used for lipidomic analysis. A total of 157 lipid species from 14 lipid classes of 4 major categories (sphingolipids, glycerophospholipids, glycerolipids, and sterols) were identified. Qualitative differences were limited to two cholesteryl ester species present only in S-sEVs. L-sEVs had higher levels of all quantified lipid classes due to their larger membrane surface area. The distribution pattern was different, especially for sphingomyelins (more in S-sEVs) and ceramides (more in L-sEVs). In conclusion, this study reveals differences in the lipidomic profile of two subsets of porcine sEVs, suggesting that they differ in biogenesis and functionality. [ABSTRACT FROM AUTHOR]

This review provides a detailed examination of CD4+ T lymphocyte subsets, crucial components of the immune system originating from the thymus. This study explores the distinct roles and mechanisms of various T helper (Th) cell subsets, including Th1, Th2, Th17, Th22, regulatory T cells (Tregs), Th9, and T follicular helper (Tfh) cells, focusing on their induction by specific cytokines, regulation by transcription factors, and the production of post-induction cytokines. The study traces the historical origins of Th lymphocyte research, emphasizing the unique cytokine profiles and functional implications of each subset in immune regulation and pathology, including autoimmune diseases, allergies, and cancer. Key findings include the delineation of cytokine-mediated induction processes, highlighting factors like interferon-gamma (IFN-γ), interleukin-4 (IL-4), transforming growth factor-beta (TGF-β), and IL-6. The review delves into transcription factors such as T-box transcription factor 21 (T-bet), GATA binding protein 3 (GATA3), and forkhead box P3 (Foxp3), underlying the lineage-specific development of these cells, and discusses the significant roles of post-induction cytokines. The research underscores the clinical relevance of CD4+ T cell subset dysregulation in various diseases, advocating for a nuanced understanding of these subsets for potential therapeutic advancements in immune-related disorders.

Background: NK cells phenotype and functional state in different genotypes of chronic viral hepatitis C (CVHC), depending on liver fibrosis severity, have not been sufficiently studied, which limits the possibilities for the development of pathology therapy. Methods: The CVHC diagnosis was based on the EASL recommendations (2018). Clinical examination with liver elastometry was performed in 297 patients with genotype 1 and in 231 patients with genotype 3 CVHC. The blood NK cells phenotype was determined by flow cytometry in 74 individuals with genotype 1 and in 69 individuals with genotype 3 CVHC. Results: The frequency of METAVIR liver fibrosis stages F3–F4 was 32.5% in individuals with genotype 3, and 20.5% in individuals with genotype 1 CVHC (p = 0.003). In patients with both genotype 1 and genotype 3 CVHC, a decrease in the total number of blood NK cells, CD56brightCD16+ NK cells and an increase in the proportion of CD56dimCD16+ NK cells, CD94+ and CD38 + CD73+ NK cells were registered in patients with fibrosis stage F3–F4 by METAVIR in comparison with persons with METAVIR fibrosis stage F0–F1. Conclusions: In patients with both genotype 1 and genotype 3 CVHC, an imbalance in the ratio between cytokine-producing and cytotoxic NK cells and an increase in the content of NK cells that express inhibitory molecules were determined in patients with severe liver fibrosis. [ABSTRACT FROM AUTHOR]

Let n ≥ 2 k ≥ 4 be integers, [ n ] k the collection of k-subsets of [ n ] = { 1 , ... , n } . Two families F , G ⊂ [ n ] k are said to be cross-intersecting if F ∩ G ≠ ∅ for all F ∈ F and G ∈ G . A family is called non-trivial if the intersection of all its members is empty. The best possible bound | F | + | G | ≤ n k - 2 n - k k + n - 2 k k + 2 is established under the assumption that F and G are non-trivial and cross-intersecting. For the proof a strengthened version of the so-called shifting technique is introduced. The most general result is Theorem 4.1. [ABSTRACT FROM AUTHOR]

Let n , k , ℓ , t be positive integers with k ≥ ℓ ≥ t + 2 and let X = X 1 ⊎ X 2 ⊎ ⋯ ⊎ X k , | X i | = n. A family F of ℓ -subsets of X is called a separated family if | F ∩ X i | ≤ 1 for all F ∈ F and i = 1 , 2 , ... , k. A separated family F is called non-trivial t -intersecting if | F ∩ F ′ | ≥ t for all F , F ′ ∈ F and | ∩ { F : F ∈ F } | < t. In the present paper, we determine the maximum size of a non-trivial t -intersecting separated family for n > (t + 1) (ℓ − t − 1) 2 (k − t − 1) + 1. [ABSTRACT FROM AUTHOR]

Neutrophils display heterogeneity and plasticity with different subgroups and immune-regulatory functions under various surrounding conditions. Neutrophils induced by IL-23/IL-18 (referred to N(IL-23+IL-18) neutrophils) have a unique gene-expression profile, with highly expressing IL-17, MHC-II, and costimulatory molecules. The adoptive transfer of N(IL-23+IL-18) neutrophils significantly increased the pathogenesis in a renal ischemia–reperfusion injury mouse model. N(IL-23+IL-18) neutrophils directly and efficiently induced allogeneic T cell proliferation in vitro. N(IL-23+IL-18) neutrophils enhanced the syngeneic T cell response to allogeneic antigens in mixed-lymphocyte reaction assays. The adoptive transfer of the donor or host N(IL-23+IL-18) neutrophils significantly enhanced the antidonor antibody production in an allogeneic-skin-transplanted mouse model, accompanied by increased Tfh cells in the spleens. Therefore, the neutrophil subset induced by IL-23/IL-18 promotes tissue injury and antidonor humoral response in the allogeneic transplantation mouse model. [ABSTRACT FROM AUTHOR]

Abstract Neutrophils, the most prevalent innate immune cells in humans, have garnered significant attention in recent years due to their involvement in cancer progression. This comprehensive review aimed to elucidate the important roles and underlying mechanisms of neutrophils in cancer from the perspective of their whole life cycle, tracking them from development in the bone marrow to circulation and finally to the tumor microenvironment (TME). Based on an understanding of their heterogeneity, we described the relationship between abnormal neutrophils and clinical manifestations in cancer. Specifically, we explored the function, origin, and polarization of neutrophils within the TME. Furthermore, we also undertook an extensive analysis of the intricate relationship between neutrophils and clinical management, including neutrophil-based clinical treatment strategies. In conclusion, we firmly assert that directing future research endeavors towards comprehending the remarkable heterogeneity exhibited by neutrophils is of paramount importance.

Seminal plasma contains a heterogeneous population of extracellular vesicles (sEVs) that remains poorly characterized. This study aimed to characterize the lipidomic profile of two subsets of differently sized sEVs, small (S-) and large (L-), isolated from porcine seminal plasma by size-exclusion chromatography and characterized by an orthogonal approach. High-performance liquid chromatography–high-resolution mass spectrometry was used for lipidomic analysis. A total of 157 lipid species from 14 lipid classes of 4 major categories (sphingolipids, glycerophospholipids, glycerolipids, and sterols) were identified. Qualitative differences were limited to two cholesteryl ester species present only in S-sEVs. L-sEVs had higher levels of all quantified lipid classes due to their larger membrane surface area. The distribution pattern was different, especially for sphingomyelins (more in S-sEVs) and ceramides (more in L-sEVs). In conclusion, this study reveals differences in the lipidomic profile of two subsets of porcine sEVs, suggesting that they differ in biogenesis and functionality.

Chronic pelvic inflammatory disease (PID) in women remains a problem due to the importance of medical consequences. The study of the receptor apparatus of neutrophilic granulocytes (NG) involved in anti-infective protection in diseases of various etiologies seems to be relevant. Aim: to clarify the features of variants of quantitative and phenotypic changes in subsets of NG CD11b+CD64-CD32+CD16+, CD11b+CD64+CD32+CD16+ of immunocompromised women during exacerbation of chronic PID of various etiologies. We were tested women 20-40 years: Study Group 1 (SG1, n = 20) – chronic PID during the exacerbation with mono- or mixed latent/recurrent various viral infections (chronic herpes-virus infections, papillomavirus infection, recurrent ARVI); Study Group 2 (SG2, n = 30) – chronic PID of bacterial etiologies; Comparison Group (CG)– 20 healthy women. The number of subsets CD11b+CD64-CD32+CD16+NG (major) and CD11b+CD64+CD32+CD16+NG (minor), receptor expression density (MFI) was determined (FC500, USA). It was found that in PID during the period of exacerbation, diagnostically significant differences in the subset composition of NG were revealed. We got a decrease in the CD11b+СD64-СD32+СD16+NG subset and in 7,6 times increase in the CD11b+CD64+CD32+CD16+NG subset in SG2 with chronic PID of bacterial etiology, in contrast to chronic PID occurring in combination with recurrent/persistent viral infection SG1. Negative transformation of NG subsets is associated with a predominant decrease in the level of expression of the activation CD16. The absence of an adequate response to the infectious and inflammatory process was revealed – the absence of an increase in the expression of the activation CD11b in the major subset in SG1, as well as in the minor subset in groups SG1 and SG2. In the major subset of NG in groups SG2 a decrease in the expression of the activation marker CD11b. In the various viral infections and PID (SG1), in the negatively altered minor subset of NG we got a decrease of expression of CD16, an increase of expression of CD64 and CD32. Determination of subsets of CD11b+СD64-СD32+СD16+, CD11b+CD64+CD32+CD16+NG and their phenotype can be used as diagnostic markers for the differential diagnosis of PID of viral and bacterial etiology, and for the development of new methods of targeted immunomodulatory therapy.

The key role of neutrophilic granulocytes (NG) in the pathogenesis of COVID-19 makes them new targets for therapeutic approaches and of influencing the course and outcome of the disease, restoring changes in the phenotype and functions of NG. Synthetic peptides or polypeptide complexes of action are the most promising in the treatment of COVID-19. Aim: to reveal the effects of the influence of the hexapeptide (HP) – Arginyl-alpha-Aspartyl-Lysyl-Valyl-Tyrosyl-Arginine on the phenotype of functionally significant NG subsets in moderate COVID-19.The study examined patients 61 (57-71) years old (n = 45) in the acute period of COVID-19 – study group1 (SG1). In vitro, samples SG1 were incubated with HP (106 g/L, 60 min, 37 °C) – study group2 (SG2). The number of NG subsets was evaluated: CD16+IFNα/βR1+CD119+, CD16+IFNα/βR1+CD119- , CD16+IFNα/βR1+CD119+, CD64- CD16+CD32+CD11b+, CD64+CD16+CD32+CD11b+ and phenotype by membrane receptor expression density (MFI) (FC 500, Beckman Coulter, USA); NG phagocytic activity was tested before and after incubation with HP. The comparison group (GS) – of 22 volunteers examined in the pre-COVID period.It was revealed that unidirectional effects of HP in vitro contributing to the restoration of the phenotype of subsets CD16+IFNα/βR1- CD119+, CD16+IFNα/βR1+CD119- to CG indicators. There was a decrease in MFI CD16 (p < 0.05) in both subsets; MFI CD119 (p < 0.05) in the CD16+IFNα/βR1- CD119+NG subset, MFI IFNa/βR1 in the CD16+IFNα/βR1+CD119- NG subset. The effects of HP on the phenotype of CD16+IFNα/βR1+CD119+NG subsets in 76% of cases were manifested by a decrease in MFI CD16 (p

Neutrophils, the most prevalent innate immune cells in humans, have garnered significant attention in recent years due to their involvement in cancer progression. This comprehensive review aimed to elucidate the important roles and underlying mechanisms of neutrophils in cancer from the perspective of their whole life cycle, tracking them from development in the bone marrow to circulation and finally to the tumor microenvironment (TME). Based on an understanding of their heterogeneity, we described the relationship between abnormal neutrophils and clinical manifestations in cancer. Specifically, we explored the function, origin, and polarization of neutrophils within the TME. Furthermore, we also undertook an extensive analysis of the intricate relationship between neutrophils and clinical management, including neutrophil-based clinical treatment strategies. In conclusion, we firmly assert that directing future research endeavors towards comprehending the remarkable heterogeneity exhibited by neutrophils is of paramount importance. [ABSTRACT FROM AUTHOR]

Several non-standard problems are regarded and the possibilities of simple approaching to their solution are regarded and discussed.

Besides its importance as a livestock species, pig is increasingly being used as an animal model for biomedical research. Macrophages play critical roles in immunity to pathogens, tissue development, homeostasis and tissue repair. These cells are also primary targets for replication of viruses such as African swine fever virus, classical swine fever virus, and porcine respiratory and reproductive syndrome virus, which can cause huge economic losses to the pig industry. In this article, we review the current status of knowledge on porcine macrophages, starting by reviewing the markers available for their phenotypical characterization and following with the characteristics of the main macrophage populations described in different organs, as well as the effect of polarization conditions on their phenotype and function. We will also review available cell lines suitable for studies on the biology of porcine macrophages and their interaction with pathogens. [ABSTRACT FROM AUTHOR]

The aim of the present study was to evaluate the subpopulation profile of T and B lymphocytes, and their relationships during therapy of the patients with Graves’ disease (GD) treated by means of radioactive iodine. We have examined 36 women with verified diagnosis of GD. The contents of thyroid hormones were determined by immunoradiometric analysis. The levels of thyroid-stimulating hormone receptor autoantibodies (rTSH) were evaluated by enzyme-linked immunosorbent assay. On the basis of comprehensive pre-therapeutic examination, all patients were exposed to the fixed-activity therapy with radioactive iodine-131 at a dose of 400 to 700 MBq administered orally in isotonic aqueous solution of sodium iodide. 56 practically healthy women were examined as a control group. The phenotype of T and B cells in whole blood was studied by flow cytometry using direct immunofluorescence. It was shown that the patients, prior to treatment with radioactive iodine, had high levels of cellular functional activity, as determined by expression of CD25 antigen on T cells and CD23-antigen on B lymphocytes. Higher functional activity of the cells responsive for adaptive immunity in the patients with GD manifests in the presence of increased levels of autoantibodies to rTSH. By means of correlation analysis, we found that the patients with GD examined before the therapy had the thyroid status may determine the functional stimulation of T and B cells, thus increasing the levels of autoimmune processes. One month after radioiodine therapy (RIT), the GD patients, along with transient hyperthyroidism with increased concentration of autoantibodies to rTSH, showed a reduction of activated T lymphocyte contents (including T helpers and cytotoxic T cells) to control values. However, the level of cytotoxic T lymphocytes in the blood remained low, and the content of Treg cells was significantly increased in the patients. Decreased contents of B cells activated memory B cell to the control levels were found in patients with GD over 1 month after RIT when studying the phenotype of blood B lymphocytes. In this case, increased levels of naive B lymphocytes and B2 cells were detected, as well as decreased numbers of activated B1 lymphocytes. The observed changes in the subpopulation composition of T and B cells, and in their phenotype developed against the background of complete absence of relationships between the studied parameters, thus suggesting loss of thyroid control of immune processes and cooperative cell interaction during the development of the immune response. Generally, the phenotypic changes of T and B lymphocyte subsets in the blood of patients with GD through 1 month after treatment with radioactive iodine may reflect a trend for decreased functional activity of adaptive cellular immunity which may also account for inhibition of autoimmune processes.

Background: NK cells phenotype and functional state in different genotypes of chronic viral hepatitis C (CVHC), depending on liver fibrosis severity, have not been sufficiently studied, which limits the possibilities for the development of pathology therapy. Methods: The CVHC diagnosis was based on the EASL recommendations (2018). Clinical examination with liver elastometry was performed in 297 patients with genotype 1 and in 231 patients with genotype 3 CVHC. The blood NK cells phenotype was determined by flow cytometry in 74 individuals with genotype 1 and in 69 individuals with genotype 3 CVHC. Results: The frequency of METAVIR liver fibrosis stages F3–F4 was 32.5% in individuals with genotype 3, and 20.5% in individuals with genotype 1 CVHC (p = 0.003). In patients with both genotype 1 and genotype 3 CVHC, a decrease in the total number of blood NK cells, CD56brightCD16+ NK cells and an increase in the proportion of CD56dimCD16+ NK cells, CD94+ and CD38 + CD73+ NK cells were registered in patients with fibrosis stage F3–F4 by METAVIR in comparison with persons with METAVIR fibrosis stage F0–F1. Conclusions: In patients with both genotype 1 and genotype 3 CVHC, an imbalance in the ratio between cytokine-producing and cytotoxic NK cells and an increase in the content of NK cells that express inhibitory molecules were determined in patients with severe liver fibrosis.

Neutrophils display heterogeneity and plasticity with different subgroups and immune-regulatory functions under various surrounding conditions. Neutrophils induced by IL-23/IL-18 (referred to N(IL-23+IL-18) neutrophils) have a unique gene-expression profile, with highly expressing IL-17, MHC-II, and costimulatory molecules. The adoptive transfer of N(IL-23+IL-18) neutrophils significantly increased the pathogenesis in a renal ischemia–reperfusion injury mouse model. N(IL-23+IL-18) neutrophils directly and efficiently induced allogeneic T cell proliferation in vitro. N(IL-23+IL-18) neutrophils enhanced the syngeneic T cell response to allogeneic antigens in mixed-lymphocyte reaction assays. The adoptive transfer of the donor or host N(IL-23+IL-18) neutrophils significantly enhanced the antidonor antibody production in an allogeneic-skin-transplanted mouse model, accompanied by increased Tfh cells in the spleens. Therefore, the neutrophil subset induced by IL-23/IL-18 promotes tissue injury and antidonor humoral response in the allogeneic transplantation mouse model.

The aim of current study was to compare profiles of T cell subsets in the patients with ankylosing spondylitis (AS) who received different modes of genetically engineered biological therapy (GEBT). The research involved 58 patients aged 20 to 58 years diagnosed with AS and treated with anti-TNFα and antiIL-17 drugs, as well as those receiving common anti-inflammatory therapy. The AS diagnostics was based on the modified New York criteria. Disease activity was assessed by means of nomenclature approved by the Assessment of Spondyloarthritis International Society and Outcome Measures in Rheumatology. 45 healthy people aged 18 to 57 were included into the control group. Peripheral blood T cell subsets were analysed by multicolor flow cytometry. It was found that the T lymphocyte subpopulation profiles in AS patients showed significant differences depending on the therapy type. First, T lymphocyte counts were decreased in AS patients receiving traditional anti-inflammatory therapy, whereas relative numbers of T cells with high levels of effector potential and cytokine secretion were increased. Negative correlations between the levels of effector memory and pre-effector cytotoxic T cells and other laboratory and clinical indexes of inflammatory activity in AS may reflect lower efficiency of traditional therapy. Next, the levels of main T cell subsets in AS patients during antiIL-17 therapy fully corresponded to the control values. However, based on numerous correlations between immunological and clinical laboratory parameters, it was concluded that anti-IL-17 therapy had an inhibitory effect on the joint inflammation activity, while the state of T cell subsets was mainly dependent on standard anti-inflammatory therapy. The most pronounced changes in T cell subsets were found in AS patients during anti-TNFα therapy was associated with decreased effector potential of Th cells and cytotoxic T lymphocytes. At the same time, the lowest frequency of extraskeletal manifestations was found in AS patients treated with anti-TNFα drugs. Finally, the higher efficiency of GEBT, compared with conventional methods of therapy, is determined by the effects upon immune targets of AS pathogenesis which manifested, e.g., by changes in the T lymphocyte subpopulation profile. Moreover, usage of anti-TNFα versus anti-IL-17 inhibitors was associated with greater effect upon phenotypic profile of T cells.

Human DCs have been divided into several subsets based on their phenotype and ontogeny. Recent high throughput single‐cell methods have revealed additional heterogeneity within human DC subsets, and new subpopulations have been proposed. In this review, we provide an updated view of the human DC subsets and of their ontogeny supported by recent clinical studies. We also summarize their main characteristics including their functional specialization. [ABSTRACT FROM AUTHOR]

Given the limited efficacy of clinical approaches that rely on ex vivo generated dendritic cells (DCs), it is imperative to design strategies that harness specialized DC subsets in situ. This requires delineating the expression of surface markers by DC subsets among individuals and tissues. Here, we performed a multiparametric phenotypic characterization and unbiased analysis of human DC subsets in blood, tonsil, spleen, and skin. We uncovered previously unreported phenotypic heterogeneity of human cDC2s among individuals, including variable expression of functional receptors such as CD172a. We found marked differences in DC subsets localized in blood and lymphoid tissues versus skin, and a striking absence of the newly discovered Axl+ DCs in the skin. Finally, we evaluated the capacity of anti-receptor monoclonal antibodies to deliver vaccine components to skin DC subsets. These results offer a promising path for developing DC subset-specific immunotherapies that cannot be provided by transcriptomic analysis alone.

We found by accident that stem cells could still be isolated from adipose tissue stored for 14 days in sealed tubes, which was distinct from previous protocols. The morphology of these hypoxia-tolerant stem cells also differs from that of conventional adipose-derived stem cells (ADSCs). In this study, we aim to define the newly found subsets. Stem cells were isolated from adipose tissue that was aspirated immediately or stored for 14 days. The stem cells were then harvested for flowcytometric analysis and differentiation potentials. The expression of hypoxia-inducible factor 1 alpha (HIF-1α) was assayed to confirm the hypoxia-tolerant ability. RNA sequencing (RNA-seq) was performed to find the common signatures of the hypoxia-tolerant cells. The result of bioinformatics was tested by quantitative real-time reverse transcription-polymerase chain reaction (qPCR) and western blotting. Certain subsets of ADSCs can be isolated from adipose tissue stored for 14 days. These survived cells were positive for CD90, CD105, and CD73 and showed multilineage differentiation potentials. The hypoxic condition was evidenced by up-regulation of HIF-1α for 2.0-fold changes (p < 0.05). The hypoxia-tolerant stem cells were distinct from multilineage-differentiating stress-enduring (Muse) cells, previously found stress-enduring stromal cells. RNA-seq suggested that integrin beta 3 (ITGB3) was highly expressed in hypoxia-tolerant subpopulations. The result was further confirmed at transcription and translation levels by qPCR and western blotting (mRNA: 2.9 ± 0.4, p < 0.05; protein: 1.5 ± 0.2, p < 0.05; respectively). The conventional ADSCs are positive for ITGB3, which implies that ITGB3+ cells are subpopulations of heterogeneous ADSCs. Our study reveals the ITGB3+ subsets with potent hypoxia tolerance, which has significant implications for improving fat retention rates and curing obesity-related diseases. [ABSTRACT FROM AUTHOR]

Introduction: Dendritic cells (DCs) are crucial to form ectopic germinal centers (GCs) in the hyperplastic thymus (HT), which are typically found in anti-acetylcholine receptor autoantibody-positive myasthenia gravis (MG) patients. However, the characteristics of such DCs in the HT and their roles in thymic hyperplasia formation remain unclear., Methods: We collected thymic tissue from MG patients and patients who underwent cardiac surgery. The tissues were cut into sections for immunohistochemistry and immunofluorescence or digested into a single cell suspension for flow cytometry., Results: In addition to formation of ectopic GCs, we found that the proportion of the medulla in the thymic parenchyma was higher than that in the cortex (area cortex /area medulla , 1.279 vs. 0.6576) in the HT of MG patients. The density of conventional dendritic cells (cDCs) in the HT was 131 ± 64.36 per mm 2 , whereas in normal thymic tissue, the density was 59.17 ± 22.54 per mm 2 . The more abundant cDCs expressed co-stimulatory molecules (CD80 and CD86) strongly. Moreover, the more abundant subset was mainly CD141+ DCs (cDC1s), accounting for an increase from 15% to 29%. However, these increased cDC1s appeared to be unrelated to Hassall's corpuscles and ectopic GCs., Conclusion: Thymic hyperplasia in MG patients is manifested as an increase in the proportion of the thymic medulla accompanied by increases in the density and functional activation as well as changes in the subset composition of cDCs., Competing Interests: Declaration of competing interest The authors have no financial conflicts of interest., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Abstract Aim IgA-producing B cells have been found to be associated with children diagnosed with Henoch-Schonlein purpura (HSP). The aim of the present study was to determine whether children with HSP possess altered B-cell subsets. Methods A total of 14 children diagnosed with HSP and age- and sex-matched healthy controls (HCs) were enrolled in our study. Peripheral blood mononuclear cells were isolated, and the percentage and absolute number of B-cell subsets and Follicular helper T (Tfh) cells were determined by flow cytometry. Finally, Spearman’s correlation coefficient was used to analyse the correlation between the percentage of Tfh cells and B-cell subsets. Results We found that compared to HCs, the frequency and absolute number of total B cells were significantly higher in children with HSP, but the percentages of plasma cells and naïve B cells were significantly lower. A significantly increased percentage and absolute number of memory nonswitched B cells were found in children with HSP compared with HCs. We observed that the expression of C-X-C chemokine receptor type 5 (CXCR5) on total CD4+ T cells and the percentage of CD4+CXCR5+ cells were significantly increased in patients with HSP. Moreover, significantly correlations between Tfh cells and various B-cell subsets were observed. Conclusions Our study showed a Tfh-cell-associated altered B cell compartment in children with HSP.

Besides its importance as a livestock species, pig is increasingly being used as an animal model for biomedical research. Macrophages play critical roles in immunity to pathogens, tissue development, homeostasis and tissue repair. These cells are also primary targets for replication of viruses such as African swine fever virus, classical swine fever virus, and porcine respiratory and reproductive syndrome virus, which can cause huge economic losses to the pig industry. In this article, we review the current status of knowledge on porcine macrophages, starting by reviewing the markers available for their phenotypical characterization and following with the characteristics of the main macrophage populations described in different organs, as well as the effect of polarization conditions on their phenotype and function. We will also review available cell lines suitable for studies on the biology of porcine macrophages and their interaction with pathogens.

The role of neutrophils in the course of Leishmania infection remains controversial, displaying tremendous variability depending on the species of parasite, stage of infection, host genetic background, and methodological discrepancies among studies. Although neutrophils have long been categorized as short‐lived cells with limited capacity to express proteins de novo, recent advances have revealed significant plasticity in neutrophil transcriptional programmes and intrapopulation heterogeneity, which can be regulated by both intrinsic and extrinsic factors that together determine the profile of neutrophil effector response. In this review, we focus on the current understanding of neutrophil transcriptional plasticity, neutrotime, evidence of Leishmania‐mediated alterations in neutrophil transcriptome leading to the rise of subpopulations, and finally, functional implications of those findings to the course of Leishmania infection. [ABSTRACT FROM AUTHOR]

Introduction: Extensive trauma surgery evokes an immediate cellular immune response including altered circulatory neutrophil numbers. The concurrent bone marrow (BM) response however is currently unclear. We hypothesize that these BM changes include (1) a relative reduction of the bone marrow neutrophil fraction and (2) increasing heterogeneity of the bone marrow neutrophil pool due to (3) the appearance of aged/returning neutrophils from circulation into the BM-compartment. Materials and Methods: Eight pigs were included in a standardized extensive trauma surgery model. Blood and bone marrow samples were collected at baseline and after 3 hours of ongoing trauma surgery. Leukocyte and subtype counts and cell surface receptor expression levels were studied by flow cytometry. Results: All animals survived the interventions. A significant drop in circulating neutrophil counts from 9.3 to 3.2x106 cells/ml (P=0.001) occurred after intervention, whereas circulatory neutrophil cell surface expression of CD11b increased. The concurrent bone marrow response included an increase of the BM neutrophil fraction from 63 ± 3 to 71 ± 3 percent (P<0.05). Simultaneously, the BM neutrophil pool became increasingly mature with a relative increase of a CXCR4high-neutrophil subtype that was virtually absent at baseline. Conclusion: The current study shows a shift in composition of the BM neutrophil pool during extensive trauma surgery that was associated with a relatively circulatory neutropenia. More specifically, under these conditions BM neutrophils were more mature than under homeostatic conditions and a CXCR4high-neutrophil subset became overrepresented possibly reflecting remigration of aged neutrophils to the BM. These findings may contribute to the development of novel interventions aimed to modify the trauma-induced immune response in the BM. [ABSTRACT FROM AUTHOR]

Evidence suggests that neutrophils exert specialized effector functions during infection and inflammation, and that these cells can affect the duration, severity, and outcome of the infection. These functions are related to variations in phenotypes that have implications in immunoregulation during viral infections. Although the complexity of the heterogeneity of neutrophils is still in the process of being uncovered, evidence indicates that they display phenotypes and functions that can assist in viral clearance or augment and amplify the immunopathology of viruses. Therefore, deciphering and understanding neutrophil subsets and their polarization in viral infections is of importance. In this review, the different phenotypes of neutrophils and the roles they play in viral infections are discussed. We also examine the possible ways to target neutrophil subsets during viral infections as potential anti-viral treatments. [ABSTRACT FROM AUTHOR]

Background: Ever since the World Health Organization (WHO) announced the SARS-CoV-2 or nCOVID-19 infection (a pandemic), continuous spread of the virus has been observed which has continuously seen to affect and kill multitudes of individuals all over the world. An understanding of the pathophysiology of this disease is necessary for an effective treatment. Laboratory investigations play an important role in the diagnosis as well as treatment of this infectious disease. Hematological parameters demonstrate alterations during the progression of nCOVID-19 infection. Of these, many are indicative of extremely poor clinical outcome. Hematological findings like leukopenia, lymphopenia, thrombocytopenia and coagulation-related abnormalities are the most common manifestations. The aim of this study was to assess the dynamic profile and clinical implications of hematological and immunological parameters among nCOVID-19 infections. Materials and Methods: This retrospective study was designed after categorizing patients suffering from COVID-19 into three groups: (a) Group I; (b) Group II and (c) Group III or severe critical patients. Hematological and immunological parameters of neutrophilic and white blood cell counts, d-dimer levels, hemoglobin levels, immunoglobulin G (IgG) and M (IgM) levels and interleukin-6 (IL-6) levels were assessed. Statistical analysis using Kruskal–Wallis test was used. Results: Normal white blood cell and neutrophil count among COVID-19 patients was seen. However, median values in Group II (P < 0.01) and Group III (P < 0.0001) were found to show significantly higher values when compared to Group I. A significant (P < 0.01) decrease in lymphocytic counts was found among severe and critical patients. Hemoglobin level was found to demonstrate higher decrease (P < 0.01) among severe and critical patients. Platelet count was found in normal range in all COVID-19 patients. Routine coagulation tests revealed increased fibrinogen (P < 0.01) and d-dimer levels (P < 0.0001) in severe and critical patients. Normal proportions of total CD3+ and CD4 + T lymphocytes were observed in COVID-19. However, CD8 + T lymphocytes proportion was found to be decreased (P-value < 0.05). Immunoglobulin G levels among Groups II and III patients were found to be lower when compared with Group I (P < 0.001). No statistical significance was observed between the groups in IgM levels. Plasma IL-6 levels were found to show progressive rise among Groups II and III patients (P < 0.05). Conclusion: Analysis of hematological and immunological parameters profiles in COVID-19 patients may help in deciphering the clinical progression of patients suffering from COVID-19 disease. Thus, regular monitoring of the hospitalized patients may help in planning the management of these cases.

IntroductionExtensive trauma surgery evokes an immediate cellular immune response including altered circulatory neutrophil numbers. The concurrent bone marrow (BM) response however is currently unclear. We hypothesize that these BM changes include (1) a relative reduction of the bone marrow neutrophil fraction and (2) increasing heterogeneity of the bone marrow neutrophil pool due to (3) the appearance of aged/returning neutrophils from circulation into the BM-compartment.Materials and MethodsEight pigs were included in a standardized extensive trauma surgery model. Blood and bone marrow samples were collected at baseline and after 3 hours of ongoing trauma surgery. Leukocyte and subtype counts and cell surface receptor expression levels were studied by flow cytometry.ResultsAll animals survived the interventions. A significant drop in circulating neutrophil counts from 9.3 to 3.2x106 cells/ml (P=0.001) occurred after intervention, whereas circulatory neutrophil cell surface expression of CD11b increased. The concurrent bone marrow response included an increase of the BM neutrophil fraction from 63 ± 3 to 71 ± 3 percent (P

Mutations in CCAAT enhancer binding protein A gene (CEBPA) are one of the common genetic alterations in acute myeloid leukemia (AML). Recently, the emergence of new evidence makes it necessary to reconsider the subsets and treatment of AML patients with CEBPA mutations. This review will summarize the history of research progress of CEBPA mutations in AML, the heterogeneities of AML with CEBPA double mutations (CEBPA dm), and two special subtypes of CEBPA mutated AML. We will discuss the treatment of AML with CEBPA mutations as well, and finally propose a new algorithm for the treatment of these patients, including both familial and sporadic CEBPA mutated AML patients. This review may be beneficial for further investigation and optimizing clinical management of AML patients with CEBPA mutations. [ABSTRACT FROM AUTHOR]

Objective: Systemic lupus erythematosus (SLE) is a complex heterogenous autoimmune disease that can affect multiple organs. We performed clinical clustering analysis to describe a lupus cohort from the University of Pittsburgh Medical Center. Methods: A total of 724 patients who met the American College of Rheumatology (ACR) classification criteria for SLE were included in this study. Clustering was performed using the ACR classification criteria and the partitioning around medoid method. Correlation analysis was performed using the Spearman's Rho test. Results: Patients with SLE in our cohort identify three district clinical disease subsets. Patients in cluster 1 were significantly more likely to develop renal and hematologic involvement, and had overrepresentation in African-American and male lupus patients. Clusters 2 and 3 identified a milder disease, with a significantly less likelihood of organ complications. Patients in cluster 2 are characterized by malar rash and photosensitivity, while patients in cluster 3 are characterized by oral ulcers, which is present in ~90% of patients within this cluster. The presence of photosensitivity or oral ulcers appears to be protective against the development of lupus nephritis in our cohort. Conclusion: We describe a large cohort of SLE from Western Pennsylvania and identify three distinct clinical disease subgroups. Clustering analysis might help to better manage and predict disease complications in heterogenous diseases like lupus. [ABSTRACT FROM AUTHOR]

Mutations in CCAAT enhancer binding protein A gene (CEBPA) are one of the common genetic alterations in acute myeloid leukemia (AML). Recently, the emergence of new evidence makes it necessary to reconsider the subsets and treatment of AML patients with CEBPA mutations. This review will summarize the history of research progress of CEBPA mutations in AML, the heterogeneities of AML with CEBPA double mutations (CEBPAdm), and two special subtypes of CEBPA mutated AML. We will discuss the treatment of AML with CEBPA mutations as well, and finally propose a new algorithm for the treatment of these patients, including both familial and sporadic CEBPA mutated AML patients. This review may be beneficial for further investigation and optimizing clinical management of AML patients with CEBPA mutations.

Background: Lymphopenia is a hallmark of multisystem inflammatory syndrome in children (MIS‐C). We aimed to characterize lymphocyte subsets' shifts and their correlations with other severity markers of MIS‐C. Methods: In this prospective cross‐sectional study, we performed peripheral lymphocyte phenotyping in 32 patients with MIS‐C. We analyzed lymphocyte subsets at three time points of the disease: the acute (A), convalescent (B), and recovery (C) phases. Based on age‐normalized lymphocyte counts, we distinguished two groups of patients: "the mild" (higher lymphocyte counts) and "the severe" (lower lymphocyte counts). In addition, we examined differences between these groups regarding other severity markers. Results: In phase A, 84% of children had lymphopenia. Decreased absolute counts of CD3, CD4, and CD8 cells were observed in, respectively, 88%, 72%, and 84% of patients. The natural killer cells were decreased in 63% and CD19 in 59% of children. "The severe" group had significantly higher procalcitonin and troponin I levels and lower platelets and albumin. Moreover, "the severe" group had hypotension more frequently (73% vs. 20%, p =.008). In phase B, all lymphocyte counts increased, and 32% of children had lymphocytosis. The increase of CD3, CD4, and CD8 counts correlated with some laboratory severity markers (hemoglobin, procalcitonin, D‐dimer, lactate dehydrogenase, N‐terminal prohormone of brain natriuretic peptide, albumin), but not with steroid use. In phase C, most children had normal lymphocyte counts. Conclusions: Substantial shifts in lymphocyte counts during MIS‐C apply most to T lymphocytes and correlate with the disease severity markers, particularly hypotension prevalence. A proportion of children with MIS‐C develops transient lymphocytosis during convalescence. [ABSTRACT FROM AUTHOR]

Although great advances have been made, the problem of irreversible myocardium loss due to the limited regeneration capacity of cardiomyocytes has not been fully solved. The morbidity and mortality of heart disease still remain high. There are many therapeutic strategies for treating heart disease, while low efficacy and high cost remain challenging. Abundant evidence has shown that both acute and chronic inflammations play a crucial role in heart regeneration and repair following injury. Macrophages, a primary component of inflammation, have attracted much attention in cardiac research in recent decades. The detailed mechanisms of the roles of macrophages in heart regeneration and repair are not completely understood, in part because of their complex subsets, various functions, and intercellular communications. The purpose of this review is to summarize the progress made in the understanding of macrophages, including recent reports on macrophage differentiation, polarization and function, and involvement in heart regeneration and repair. Also, we discuss progress in treatments, which may suggest directions for future research.

Objective: Recent studies on follicular regulatory T (Tfr) and follicular helper T (Tfh) cells suggest that they may participate in the pathogenesis of rheumatoid arthritis (RA). Here, we examine Tfr-like and Tfh-like cells and their subsets in RA and assess the correlations between these subsets with B cells and cytokines related to the pathogenesis of RA and their clinical significance.Methods: The study population consisted of 18 healthy controls and 47 RA patients (17 new onset, 57.00 ± 11.73 years; 30 treated RA patients, 57.56 ± 1.97 years). Disease activity scores in 28 joints were calculated. The positive rates of rheumatoid factor (RF) and anticyclic citrullinated peptide antibodies (anti-CCP) were 82.9 and 89.4%, respectively. Cell subsets were analyzed using flow cytometry, and serum cytokine levels were measured using cytometric bead array.Results: Tfh-like and PD-1+ Tfh-like cells were elevated, and the distribution of Tfh-like cell subsets was altered with increased Tfh17-like and Tfh1/17-like cells in RA patients. The receiver operating characteristics curves for Tfh-like, Tfh17-like, Tfh1/17-like, and PD-1+ Tfh-like cells indicate improved RA diagnostic potential. RA patients had decreased regulatory T (Treg), Tfr-like, and memory Tfr-like (mTfr-like) cells and increased Tfh-like/Treg, Tfh-like/Tfr-like, and Tfh-like/mTfr-like cell ratios. Tfh-like cells and their subsets, including Tfh1-like, Tfh2-like, Tfh1/17-like, and PD-1+ Tfh-like cells, were positively correlated with B cells. Tfh-like/Treg, Tfh-like/Tfr-like, and Tfh-like/mTfr-like cell ratios were positively correlated with B cells in new-onset RA. Interleukin (IL)-2, IL-4, IL-17, interferon-γ, and tumor necrosis factor-α were positively correlated with Tfr-like and mTfr-like cells. IL-2 and IL-10 were positively correlated with Tfh-like and Tfh2-like cells. IL-4 was positively correlated with Tfh-like cells.Conclusions: Tfh-like and PD-1+ Tfh-like cells are increased, whereas Treg, Tfr-like, and mTfr-like cells are decreased in RA, leading to an imbalance in Tfh-like/Treg, Tfh-like/Tfr-like, and Tfh-like/mTfr-like cell ratios. Tfh-like cells and a portion of their subsets as well as Tfh-like/Treg, Tfh-like/Tfr-like, and Tfh-like/mTfr-like cell ratios are closely related to B cells. Dysfunction of cell subsets leads to abnormal levels of cytokines involved in the pathogenesis of RA. The altered distributions of Tfh-like cell subsets, especially Tfh1/17-like cells, represent potential therapeutic targets for treatment of RA.

Background: Ever since the World Health Organization (WHO) announced the SARS-CoV-2 or nCOVID-19 infection (a pandemic), continuous spread of the virus has been observed which has continuously seen to affect and kill multitudes of individuals all over the world. An understanding of the pathophysiology of this disease is necessary for an effective treatment. Laboratory investigations play an important role in the diagnosis as well as treatment of this infectious disease. Hematological parameters demonstrate alterations during the progression of nCOVID-19 infection. Of these, many are indicative of extremely poor clinical outcome. Hematological findings like leukopenia, lymphopenia, thrombocytopenia and coagulation-related abnormalities are the most common manifestations. The aim of this study was to assess the dynamic profile and clinical implications of hematological and immunological parameters among nCOVID-19 infections. Materials and Methods: This retrospective study was designed after categorizing patients suffering from COVID-19 into three groups: (a) Group I; (b) Group II and (c) Group III or severe critical patients. Hematological and immunological parameters of neutrophilic and white blood cell counts, d-dimer levels, hemoglobin levels, immunoglobulin G (IgG) and M (IgM) levels and interleukin-6 (IL-6) levels were assessed. Statistical analysis using Kruskal–Wallis test was used. Results: Normal white blood cell and neutrophil count among COVID-19 patients was seen. However, median values in Group II (P < 0.01) and Group III (P < 0.0001) were found to show significantly higher values when compared to Group I. A significant (P < 0.01) decrease in lymphocytic counts was found among severe and critical patients. Hemoglobin level was found to demonstrate higher decrease (P < 0.01) among severe and critical patients. Platelet count was found in normal range in all COVID-19 patients. Routine coagulation tests revealed increased fibrinogen (P < 0.01) and d-dimer levels (P < 0.0001) in severe and critical patients. Normal proportions of total CD3+ and CD4 + T lymphocytes were observed in COVID-19. However, CD8 + T lymphocytes proportion was found to be decreased (P-value < 0.05). Immunoglobulin G levels among Groups II and III patients were found to be lower when compared with Group I (P < 0.001). No statistical significance was observed between the groups in IgM levels. Plasma IL-6 levels were found to show progressive rise among Groups II and III patients (P < 0.05). Conclusion: Analysis of hematological and immunological parameters profiles in COVID-19 patients may help in deciphering the clinical progression of patients suffering from COVID-19 disease. Thus, regular monitoring of the hospitalized patients may help in planning the management of these cases. [ABSTRACT FROM AUTHOR]

It is now becoming clear that neutrophils and eosinophils are heterogeneous cells with potentially multiple subsets in health and disease. With greater marker coverage by multi-color flow cytometry and single-cell level sequencing of granulocyte populations, novel phenotypes of these cells began to emerge. Intriguingly, many newly described subsets blend distinctions between classical myeloid lineage phenotypes, which are especially true for tissue resident or recruited cells in contexts of inflammation and disease. This includes reports of neutrophils with features of eosinophils, monocytes and dendritic cells, and eosinophil subsets expressing neutrophil markers. Moreover, novel studies show the ability of immature neutrophils to transdifferentiate into mature cells belonging to other myeloid lineages (eosinophils, monocytes/macrophages). In this review, we summarize novel findings in this exciting research frontier and shed light on potential processes driving the plasticity and heterogeneity of granulocyte subsets. Specifically, we discuss the hematopoietic flexibility of granulocyte precursors in bone marrow and the adaptation of myeloid cells to local tissue microenvironments. The understanding of such intermediate and developmental phenotypes is very important, as it can teach us about origins of functionally distinct myeloid cells during inflammation, and explain reasons for successes and failures of biologics targeting terminally differentiated granulocytes. [ABSTRACT FROM AUTHOR]

Recent studies suggest that murine invariant natural killer T (iNKT) cell development culminates in three terminally differentiated iNKT cell subsets denoted as NKT1, 2, and 17 cells. Although these studies corroborate the significance of the subset division model, less is known about the factors driving subset commitment in iNKT cell progenitors. In this review, we discuss the latest findings in iNKT cell development, focusing in particular on how T-cell receptor signal strength steers iNKT cell progenitors toward specific subsets and how early progenitor cells can be identified. In addition, we will discuss the essential factors for their sustenance and functionality. A picture is emerging wherein the majority of thymic iNKT cells are mature effector cells retained in the organ rather than developing precursors.

Evidence suggests that neutrophils exert specialized effector functions during infection and inflammation, and that these cells can affect the duration, severity, and outcome of the infection. These functions are related to variations in phenotypes that have implications in immunoregulation during viral infections. Although the complexity of the heterogeneity of neutrophils is still in the process of being uncovered, evidence indicates that they display phenotypes and functions that can assist in viral clearance or augment and amplify the immunopathology of viruses. Therefore, deciphering and understanding neutrophil subsets and their polarization in viral infections is of importance. In this review, the different phenotypes of neutrophils and the roles they play in viral infections are discussed. We also examine the possible ways to target neutrophil subsets during viral infections as potential anti-viral treatments.

• Phenotype of Tph17 cells is activated and proliferative in psoriasis vulgaris. • Tph17 cells and plasma CXCL13 could be biomarkers for evaluating the severity of psoriasis vulgaris. • Tph17 cells and the CXCL13/CXCR5 axis might represent new immunotherapeutic targets for psoriasis vulgaris. Recently, a new subgroup of T cells, named peripheral helper T (Tph) cells, has been implicated in autoimmune pathogenesis. An imbalance of Tph cell subsets influences the severity of immune-related diseases. However, the characteristics and roles of Tph cell subsets in psoriasis remain unknown. Programmed cell death 1-positive, chemokine C-X-C receptor (CXCR) 5-negative Tph cells can be divided into 3 subgroups based on differential expression of chemokine CXCR3 and chemokine C-C receptor (CCR) 6. CXCR3+CCR6− Tph cells are classified as Tph1, CXCR3−CCR6− Tph cells are classified as Tph2, and CXCR3−CCR6+ Tph cells are classified as Tph17. In this study, conditions of circulating Tph cell subsets and CD4+CXCR5+ follicular helper T (Tfh) cells in 27 patients with psoriasis and 13 healthy individuals were detected by flow cytometry. The level of plasma chemokine C-X-C ligand (CXCL) 13 was measured by enzyme-linked immunosorbent assay. The correlations between the above indexes and disease severity were explored. In the peripheral blood of patients with psoriasis, Tph17 cells had an activated, proliferative phenotype; the quantity of the cells correlated with disease severity. Plasma CXCL13 levels were elevated in psoriasis and associated with disease severity and the frequency of Tph17 cells. CD4+CXCR5+ Tfh cells were increased in patients and positively correlated with disease severity, the frequency of Tph17 cells, and plasma CXCL13 levels. Our results suggest that Tph17 cells and the CXCL13/CXCR5 axis may be involved in the pathogenesis of psoriasis and represent new immunotherapeutic targets for treating psoriasis. [ABSTRACT FROM AUTHOR]

Ordinal classifier cascades are constrained by a hypothesised order of the semantic class labels of a dataset. This order determines the overall structure of the decision regions in feature space. Assuming the correct order on these class labels will allow a high generalisation performance, while an incorrect one will lead to diminished results. In this way ordinal classifier systems can facilitate explorative data analysis allowing to screen for potential candidate orders of the class labels. Previously, we have shown that screening is possible for total orders of all class labels. However, as datasets might comprise samples of ordinal as well as non-ordinal classes, the assumption of a total ordering might be not appropriate. An analysis of subsets of classes is required to detect such hidden ordinal substructures. In this work, we devise a novel screening procedure for exhaustive evaluations of all order permutations of all subsets of classes by bounding the number of enumerations we have to examine. Experiments with multi-class data from diverse applications revealed ordinal substructures that generate new and support known relations. [ABSTRACT FROM AUTHOR]

IntroductionRenal relapses adversely affect the long-term outcomes of patients with lupus nephritis (LN), but the pathogenic mechanisms remain elusive. B cell signatures of miR-148a, BACH1, BACH2, and PAX5 expression are relevant to the regulation of B lymphocyte homeostasis. It is unknown whether B cell signature is related to the relapse of LN.MethodsWe compared B lymphocyte subsets and cellular signatures during disease quiescence between LN patients with multiple relapses (MR, ≥3 LN relapses within 36 months) and those with no relapse (NR). Also, circulating B lymphocytes were isolated from treatment-naïve patients with active LN and treated with antagomir-148a in vitro to investigate the relationship between miR-148a, BACH1, BACH2, and PAX5.ResultsMR patients (n = 19), when compared with NR (n = 14), showed significantly lower percentage of circulating naïve B cells and higher memory B cell-to-naïve B cell ratio. MR patients also showed higher miR-148a levels in sera and B cells, and lower BACH1, BACH2, and PAX5 expression in naïve and memory B cells. Antagomir-148a upregulated BACH1, BACH2, and PAX5 expression, and reduced B cell proliferation upon stimulation, in naïve and memory B cells isolated from treatment-naïve active LN patients.ConclusionAltered B cell subsets and cellular signatures of miR-148a, BACH1, BACH2, and PAX5 may be associated with distinct patient phenotypes related to the risk of LN relapse.

Bone is capable of regeneration after injury, but the process of properly restoring form and function is highly complex and prone to failure. The restoration process requires highly ordered and sequential interplay at the injury site between the host immune system and bone tissue. The dynamic process that occurs after bone injury includes the formation of a hematoma, the development of an inflammatory response and callus, and the remodeling of newly formed bone tissue. The inflammatory response at the injury site is essential for the onset of bone regeneration. This inflammatory response is tightly linked with the host immune system, in which various immune cells and molecules are involved. Recently, the relationship between T cells and bone regeneration has become a popular topic; however, currently, there are no summaries of the relationship between T cells and bone regeneration. Thus, this review aimed to elucidate the modulatory functions of T cells in bone regeneration.

Here, a novel structure-preserving filtering based method is proposed for feature extraction of hyperspectral images (HIs). In the first step, the authors partition the HI into several subsets of neighbouring bands and then fuse the bands in each subset by averaging method. Second, the resulting features are obtained by bilateral texture filtering (BTF) on the fused bands. BTF is a structure-preserving filtering technology, which aims at removing texture while preserving main structure information of source image. Finally, the SVM classifier is performed on the filtered image to obtain the classification result. Experiments tested on two popular hyperspectral data sets show that the proposed method outperforms some other widely used methods.

Introduction: Renal relapses adversely affect the long-term outcomes of patients with lupus nephritis (LN), but the pathogenic mechanisms remain elusive. B cell signatures of miR-148a, BACH1, BACH2, and PAX5 expression are relevant to the regulation of B lymphocyte homeostasis. It is unknown whether B cell signature is related to the relapse of LN. Methods: We compared B lymphocyte subsets and cellular signatures during disease quiescence between LN patients with multiple relapses (MR, ≥3 LN relapses within 36 months) and those with no relapse (NR). Also, circulating B lymphocytes were isolated from treatment-naïve patients with active LN and treated with antagomir-148a in vitro to investigate the relationship between miR-148a, BACH1, BACH2, and PAX5. Results: MR patients (n = 19), when compared with NR (n = 14), showed significantly lower percentage of circulating naïve B cells and higher memory B cell-to-naïve B cell ratio. MR patients also showed higher miR-148a levels in sera and B cells, and lower BACH1, BACH2, and PAX5 expression in naïve and memory B cells. Antagomir-148a upregulated BACH1, BACH2, and PAX5 expression, and reduced B cell proliferation upon stimulation, in naïve and memory B cells isolated from treatment-naïve active LN patients. Conclusion: Altered B cell subsets and cellular signatures of miR-148a, BACH1, BACH2, and PAX5 may be associated with distinct patient phenotypes related to the risk of LN relapse. [ABSTRACT FROM AUTHOR]

Here, a novel structure-preserving filtering based method is proposed for feature extraction of hyperspectral images (HIs). In the first step, the authors partition the HI into several subsets of neighbouring bands and then fuse the bands in each subset by averaging method. Second, the resulting features are obtained by bilateral texture filtering (BTF) on the fused bands. BTF is a structure-preserving filtering technology, which aims at removing texture while preserving main structure information of source image. Finally, the SVM classifier is performed on the filtered image to obtain the classification result. Experiments tested on two popular hyperspectral data sets show that the proposed method outperforms some other widely used methods. [ABSTRACT FROM AUTHOR]