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Systemic lupus erythematosus (SLE) is a chronic autoimmune disease of unknown aetiology, with the broad range of antibodies affecting various organs and tissues, leading to rapid disability and even to lethal outcome. Our objective was to make an analysis of the results of relevant global studies about genetic mutations, spectrum of antibodies and cytokines involved in the pathogenesis of SLE. The search was conducted in PubMed and Google Scholar platforms using keywords “systemic lupus erythematosus”, “genetic mutations”, “autoantibodies”, “cytokine production”, “sequencing”, “NGS" and "exome". Several genes were found to be involved in the pathogenesis of SLE, the majority of which were associated with B- and T-cell abnormal activation. The results of different studies revealed an association of active SLE with the increase in specific circulating autoantibodies. Based on the results of the current review, a preliminary list of autoantibodies, genes and cytokines associated with the development of SLE was prepared. Future directions will include the assessment of association of genes, antibodies and cytokines in SLE patients from the local Kazakh population, and the development of genetic-immunologic panel for the early diagnosis of this disease.

Ángela María Giraldo-Montoya,1,2,&ast; Carlos A Torres-Duque,1,3,&ast; Luis F Giraldo-Cadavid,4,5 Maria E Laucho-Contreras,1 Angélica González-Flórez,1 Ana María Santos,3 Eduardo A Tuta-Quintero,1,5 Bartolomé R Celli,6 Mauricio González-García1,7 1CINEUMO, Research Center, Fundación Neumológica Colombiana, Bogotá, Colombia; 2School of Medicine, Universidad Tecnológica de Pereira, Pereira, Colombia; 3Biosciences Doctoral, Universidad de La Sabana, Chía, Colombia; 4Medical Department, Fundación Neumológica Colombiana, Bogotá, Colombia; 5Epidemiology and Biostatistics Department, Universidad de La Sabana, Chía, Colombia; 6Harvard Medical School, Boston, MA, USA; 7School of Medicine, Universidad de La Sabana, Chía, Colombia&ast;These authors contributed equally to this workCorrespondence: Carlos A Torres-Duque, Research Department, Fundación Neumológica Colombiana, Bogotá, Colombia, Biosciences Doctoral, Universidad de La Sabana, Chía, Colombia, Email ctorres@neumologica.orgIntroduction: There is a need to better understand the etiotypes of chronic obstructive pulmonary disease (COPD) beyond the tobacco-smoke (TS-COPD). Wood smoke COPD (WS-COPD) is characterized by greater airway compromise, milder emphysema, and slower rate of lung function decline than TS-COPD. However, it is unclear if these two etiotypes of COPD have differences in sputum biomarker concentrations. Objective was to compare sputum levels of selected sputum biomarkers between WS-COPD and TS-COPD, and healthy controls.Methods: Eighty-eight women (69± 12 years) were recruited and classified into: WS-COPD (n=31), TS-COPD (n=29) and controls (n=28). Using ELISA, we determined induced sputum levels of metalloproteinase 9 (MMP-9), chemokine ligand 5 (CCL5), interleukin-8 (IL-8), chemokine ligand 16 (CCL16/HCC-4) and vascular endothelial growth factor (VEGF-1). Differences were analyzed by Kruskal–Wallis and Mann–Whitney-U tests and correlation between airflow limitation and biomarkers by Spearman’s test.Results: At similar degree of airflow obstruction, anthropometrics and medications use, the level of sputum CCL5 was higher in TS-COPD than WS-COPD (p=0.03) without differences in MMP-9, IL-8, CCL16/HCC-4, and VEGF-1. Women with WS-COPD and TS-COPD showed significantly higher sputum levels of MMP-9, IL-8 and CCL5 compared with controls (p< 0.001). FEV1% predicted correlated negatively with levels of MMP-9 (rho:-0.26; P=0.016), CCL5 (rho:-0.37; P=0.001), IL-8 (rho:-0.42; P< 0.001) and VEGF (rho:-0.22; P=0.04).Conclusion: While sputum concentrations of MMP-9, IL-8, and CCL5 were higher in COPD women compared with controls, women with TS-COPD had higher levels of CCL5 compared with those with WS-COPD. Whether this finding relates to differences in pathobiological pathways remains to be determined.Keywords: COPD, wood smoke, biomass fuels, tobacco smoke, biomarkers, sputum, cytokines

Osteoarthritis is caused by a complex interplay of genetic, metabolic, immunological, inflammatory, biochemical, and biomechanical factors. In recent years, a fairly large number of studies have been devoted to the role of cellular factors of the immune system in the development of osteoarthritis. The aim of the study was to analyze scientifc publications devoted to the study of cellular factors in the pathogenesis of osteoarthritis and to assess their signifcance in the development of joint pathology. Material and methods. The search for publications by keywords was carried out in the PubMed, Google Scholar, eLibrary databases and specialized journals related to therapy, rheumatology, traumatology and immunology from 2000 to 2022. Results and discussion. Summarizing modern ideas about the role of cellular factors of the immune system in the pathogenesis of osteoarthritis, it is necessary to note the presence of synovial inflammation, a key role in the development of which is assigned to macrophages. At the same time, patients with osteoarthritis are characterized by the predominance of classically activated macrophages with a pronounced pro-inflammatory effect. In addition, T lymphocytes also play an important role in the pathogenesis of joint damage. Among them, a special role is given to T helper cells, cytotoxic T lymphocytes and memory T cells. An imbalance of cytokines and chemokines produced by subpopulations of T lymphocytes is the reason for triggering a number of mechanisms for the onset and progression of osteoarthritis. A signifcant role in the development and progression of osteoarthritis is also assigned to neutrophils, which contribute to the development of inflammation. Neutrophil-produced elastase enhances cartilage degradation, chondrocyte apoptosis, unbalanced subchondral bone remodeling, and osteophyte formation. Conclusions. Knowledge of the role of cellular immune factors in the pathogenesis of osteoarthritis and ways to implement their effects determines the prospects for the use of immunotropic agents. Also, it should be taken into account that the occurrence and progression of osteoarthritis is due to the simultaneous combination of the influence of a wide range of various components, including risk factors, traumatic joint injury, etc.

Background and Aims: Necrotizing enterocolitis (NEC) is a life-threatening disease and the most common gastrointestinal emergency in premature infants. Accurate early diagnosis is challenging. Modified Bell’s staging is routinely used to guide diagnosis, but early diagnostic signs are nonspecific, potentially leading to unobserved disease progression, which is problematic given the often rapid deterioration observed. We investigated fecal cytokine levels, coupled with gut microbiota profiles, as a noninvasive method to discover specific NEC-associated signatures that can be applied as potential diagnostic markers. Methods: Premature babies born below 32 weeks of gestation were admitted to the 2-site neonatal intensive care unit (NICU) of Imperial College hospitals (St. Mary’s or Queen Charlotte’s & Chelsea) between January 2011 and December 2012. During the NICU stay, expert neonatologists grouped individuals by modified Bell’s staging (healthy, NEC1, NEC2/3) and fecal samples from diapers were collected consecutively. Microbiota profiles were assessed by 16S rRNA gene amplicon sequencing and cytokine concentrations were measured by V-Plex multiplex assays. Results: Early evaluation of microbiota profiles revealed only minor differences. However, at later time points, significant changes in microbiota composition were observed for Bacillota (adj. P = .0396), with Enterococcus being the least abundant in Bell stage 2/3 NEC. Evaluation of fecal cytokine levels revealed significantly higher concentrations of IL-1α (P = .045), IL-5 (P = .0074), and IL-10 (P = .032) in Bell stage 1 NEC compared to healthy individuals. Conclusion: Differences in certain fecal cytokine profiles in patients with NEC indicate their potential use as diagnostic biomarkers to facilitate earlier diagnosis. Additionally, associations between microbial and cytokine profiles contribute to improving knowledge about NEC pathogenesis.

Introduction: Monitoring changes in the levels of immune markers is of great significance in evaluating the effectiveness of treatment in patients with allergic rhinitis. Objectives: Determine the change in the concentration of immune markers after treatment in patients with allergic rhinitis caused by cotton dust. Methods : A descriptive, single-group, comparative before and after intervention study on 52 patients with allergic rhinitis caused by cotton dust. Comparison of immunological markers results before and after 36 months of treatment. Results: Total IgE concentration after treatment decreased, the median decreased from 1227.756 U/mL to 676.805 UI/mL. Serum levels of IgG, IgG4, and IgG1 in patients after treatment increased compared to before (p< 0.001). The cytokines also changed in the direction of no longer responding toward allergy. Median IL-17 decreased from 1.752 mg/dL to 0.417 mg/dL. Conclusion: In patients with allergic rhinitis after specific sublingual desensitization treatment, IgE levels and cytokines such as IL-6 and IL-17 are significantly reduced and IgG, IgG4 and IgG1 levels are increased after treatment.

Our objective was to investigate the inflammatory and oxidative stress markers in patients with moderate and severe form of COVID-19. In addition, we show the correlation between changes in lymphocyte subsets and markers of oxidative stress as a tool for patient classification. IL-6 and VEGF were analysed by utilizing a High Sensitivity Evidence Investigator™ Biochip Array technology. The total antioxidant capacity (PAT) and the free radical concentrations (d-ROM) were measured in serum utilizing analytical photometric system FRAS5. Peripheral blood was used to determine CD45 + mononuclear, B, T, and NK cells using a multi-parameter flow cytometric immunophenotypic test. Statistically significant differences in IL-6 and VEGF levels were observed between the two patient groups. Decreased values of the absolute number of lymphocytes and their CD4 + and CD8 + positive T cells, NK cells, and CD8 were obtained. In the moderate group, good correlations were found between IL-6 and VEGF and NK cells (r = 0.6973, p

Lead toxicity elicits neurological damage which is a well-known disorder that has been considered to be a major cause for multiple condition such as behavioral defect; mental retardation; and nerve insufficient activity. This research is designed to estimate potential protective effect of vinpocetine on neurotoxicity stimulated by lead acetate in rats. Eighteen adult rats of both sexes were randomly enrolled into three groups. Each group includes 6 rats as followings: Group I- Rats were given 0.3ml normal saline solution orally; then intraperitoneal injection of 100μl of the normal saline was given 1h later; this group was considered as control. Group II- Rats were given an intraperitoneal injection of 20mg/kg lead acetate for 5 days. Group III- Rats were orally given 3mg/kg vinpocetine, which was given 1hr before [(the IP injection of Pb every 24 hours at a dose of 20mg/kg) for 5 days and continued for 10 days]. On 11th day of the study, the brain of each animal has been surgically cut-out to make homogenate preparation to estimate tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-10 (IL-10) levels. Lead significantly elevated TNF-α and IL-1beta; while, it significantly decreased IL-10 levels. Vinpocetine significantly minimized IL-1beta and TNF-α; furthermore, vinpocetine significantly raise IL-10 levels at (P

MicroRNAs are small non-coding RNA regulatory molecules that play an important role in the development and function of immune cells. MicroRNA-26a (miR-26a) exhibits anti-inflammatory immune effects on immune cells. However, the exact mechanism by which miR-26a plays an anti-inflammatory role remains unclear. Here, we report that miR-26a reduces inflammatory response via inhibition of prostaglandin E2 (PGE2) production by targeting cyclooxygenase-2 (COX-2). We found that miR-26a was downregulated in vitro and in vivo. The miR-26a mimic significantly decreased COX-2 protein levels, further inhibiting pro-inflammatory cytokine production in LPS-stimulated macrophages. We predicted that miR-26a could potentially target COX-2 in LPS-stimulated macrophages. Computational algorithms showed that the 3′-UTR of COX-2 mRNA contains a binding site for miR-26a. This putative targeting relationship between miR-26a and COX-2 was further confirmed by a dual-reporter gene assay. The anti-inflammatory effects of the miR-26a mimic were diminished by PGE2 supplementation. Importantly, miR-26a mimics protected mice from lethal endotoxic shock and attenuated pro-inflammatory cytokine production. Collectively, these results suggest that miR-26a may function as a novel feedback negative regulator of the hyperinflammatory response and as a drug target for the progression of inflammation. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to investigate the potential therapeutic efficacy of rutin in the management of psoriasis and elucidate its underlying molecular mechanisms., Methods: A systems biology approach, utilizing network pharmacology, was employed to identify and analyze putative targets of rutin relevant to psoriasis. The impact of rutin on the Psoriasis Area and Severity Index (PASI) scores was assessed in an imiquimod (IMQ)-induced murine psoriasis model. Histopathological alterations in the skin lesions were examined using hematoxylin and eosin (H&E) staining. Expression levels of key inflammatory mediators, including Tnf, Hif1a, Ptgs2, Tlr4, Nfkb1, Mtor, and Il2, were quantified using quantitative real-time polymerase chain reaction (qRT-PCR)., Results: A comprehensive analysis revealed 62 potential targets of rutin in the context of psoriasis, with these targets being part of 72 interconnected signaling pathways. In vivo studies demonstrated a significant reduction in PASI scores in rutin-treated mice compared to those in the control group. Additionally, rutin treatment was associated with marked improvements in skin lesions, characterized by reduced crust formation and epidermal thickness. qRT-PCR analysis indicated that rutin administration downregulated the mRNA expression of Tnf, Hif1a, Ptgs2, Tlr4, Nfkb1, Mtor, and Il2 in the lesional skin., Conclusion: These findings suggest that rutin holds promise as a therapeutic agent for psoriasis, as it effectively ameliorates IMQ-induced psoriasis-like skin inflammation in mice through modulation of multiple signaling pathways and inflammatory mediators., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Introduction: The macrophage migration inhibitory factor (MIF) plays a pivotal role in the development of rheumatoid arthritis (RA). Previous research indicates that MIF can trigger the expression of cytokine profiles associated with Th1, Th2, and Th17 responses in peripheral blood mononuclear cells (PBMC) from both RA patients and control subjects (CS). Despite these, few studies to date precisely elucidate the molecular mechanisms involved. The present study aimed to associate the expression of Th differentiation TF (T-bet, GATA-3, RORγt) with MIF receptors (CD44, CD74, CXCR2, 4, 7) and Th1, Th2, and Th17 cytokines in PBMC from CS and RA patients., Method: PBMC from both groups was cultured for 24 h. The expression of the canonical and non-canonical MIF receptors and the TF was determined by flow cytometry. Additionally, multiplex bead analysis was employed to assess the levels of cytokines in the culture supernatants. The findings revealed that T CD4+ lymphocytes in the CS group exhibited a heightened expression of CD74 (p<0.05), whereas RA patients displayed an elevated expression of CXCR7 (p<0.001). Furthermore, T CD4+ lymphocytes from RA patients exhibited greater expression of GATA3, RORγt, and FOXP3, along with elevated levels of pro-inflammatory cytokines compared to the CS group (p<0.001)., Result: These results indicate that CD74 is more prominently expressed in PBMC from the CS group, whereas CXCR7 is more expressed in PBMC from RA patients., Conclusion: We also noted an increased secretion of Th17 profile cytokines in RA, potentially influenced by the activation of FOXP3 via CD74 and RORγt through CXCR7 using the endocytic pathway., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Tumor metastasis is a complex process that is controlled at the molecular level by numerous cytokines. Primary breast and prostate tumors most commonly metastasize to bone, and the development of increasingly accurate targeted nanocarrier systems has become a research focus for more effective anti-bone metastasis therapy. This review summarizes the molecular mechanisms of bone metastasis and the principles and methods for designing bone-targeted nanocarriers and then provides an in-depth review of bone-targeted nanocarriers for the treatment of bone metastasis in the context of chemotherapy, photothermal therapy, gene therapy, and combination therapy. Furthermore, this review also discusses the treatment of metastatic and primary bone tumors, providing directions for the design of nanodelivery systems and future research., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Systemic Sclerosis (SSc) is a systemic autoimmune disease of unknown etiology with a highly complex pathogenesis that despite extensive investigation is not completely understood. The clinical and pathologic manifestations of the disease result from three distinct processes: 1) Severe and frequently progressive tissue fibrosis causing exaggerated and deleterious accumulation of interstitial collagens and other extracellular matrix molecules in the skin and various internal organs; 2) extensive fibroproliferative vascular lesions affecting small arteries and arterioles causing tissue ischemic alterations; and 3) cellular and humoral immunity abnormalities with the production of numerous autoantibodies, some with very high specificity for SSc. The fibrotic process in SSc is one of the main causes of disability and high mortality of the disease. Owing to its essentially universal presence and the severity of its clinical effects, the mechanisms involved in the development and progression of tissue fibrosis have been extensively investigated, however, despite intensive investigation, the precise molecular mechanisms have not been fully elucidated. Several recent studies have suggested that cellular transdifferentiation resulting in the phenotypic conversion of various cell types into activated myofibroblasts may be one important mechanism. Here, we review the potential role that cellular transdifferentiation may play in the development of severe and often progressive tissue fibrosis in SSc., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

In the past decades, scientists have made outstanding efforts to treat diabetes. However, diabetes treatment is still far from satisfactory due to the complex nature of the disease and the challenges encountered in resolving it. Inflammatory factors are key regulators of the immune system's response to pathological insults, organ neogenesis, rejuvenation of novel cells to replace injured cells and overwhelming disease conditions. Currently, the available treatments for type 1 diabetes include daily insulin injection, pancreatic beta cell or tissue transplantation, and gene therapy. Cell therapy, exploiting differentiation, and reprogramming various types of cells to generate pancreatic insulin-producing cells are novel approaches for the treatment of type 1 diabetes. A better understanding of the inflammatory pathways offers valuable and improved therapeutic options to provide more advanced and better treatments for diabetes. In this review, we investigated different types of inflammatory factors that participate in the pathogenesis of type 1 diabetes, their possible dual impacts on the differentiation, reprogramming, and fusion of other stem cell lines into pancreatic insulin-producing beta cells, and the possibility of applying these factors to improve the treatment of this disease., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: Renal disease in T2DM could arise independently of hyperglycemia, aka non diabetic kidney disease. Its prevalence ranges from 33% to 72.5% among T2DM patients. Specific molecular signatures that distinguish Diabetic Nephropathy from NDKD (FSGS) in T2DM might provide new targets for CKD management., Methods: Five original GEO microarray DN and FSGS datasets were evaluated (GSE111154, GSE96804, GSE125779, GSE129973 and GSE121233). Each of the three groups (DN, FSGS, and Controls) had equal renal transcriptome data (n=32) included in the analysis to eliminate bias. The DEGs were identified using TAC4.0. Pathway analysis was performed on the discovered genes aligned to official gene symbols using Reactome, followed by functional gene enrichment analysis using Funrich, Enrichr..STRING and Network analyst investigated PPI, followed by Webgestalt's pathway erichment. Finally, using the Targetscan 7.0 and DIANA tools, filtered differential microRNAs downregulated in DN were evaluated for target identification., Result: Between the three groups, DN, FSGS, and Control, a total of 194 DEGs with foldchange, >2 & <-2 and P-value 0.01 were found in the renal transcriptome. In comparison to control, 45 genes were elevated, particularly in DN, whereas 43 were upregulated specifically in FSGS. DN datasets were compared to FSGS in a separate analysis. FABP4, EBF1, ADIRF, and ART4 were shown to be among the substantially up-regulated genes unique to DN in both analyses. The transcriptional regulation of white adipocytes was discovered by pathway analysis., Conclusion: The molecular markers revealed might be employed as specific targets in the aetiology of DN, as well as in T2DM patients' therapeutic care., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background: The IL-17 (interleukin 17) family consists of six structurally related pro-inflammatory cytokines, namely IL-17A to IL-17F. These cytokines have garnered significant scientific interest due to their pivotal role in the pathogenesis of various diseases. Notably, a specific subset of T-cells expresses IL-17 family members, highlighting their importance in immune responses against microbial infections., Introduction: IL-17 cytokines play a critical role in host defense mechanisms by inducing cytokines and chemokines, recruiting neutrophils, modifying T-cell differentiation, and stimulating the production of antimicrobial proteins. Maintaining an appropriate balance of IL-17 is vital for overall health. However, dysregulated production of IL-17A and other members can lead to the pathogenesis of numerous inflammatory and autoimmune diseases., Method: This review provides a comprehensive overview of the IL-17 family and its involvement in several inflammatory and autoimmune diseases. Relevant literature and research studies were analyzed to compile the data presented in this review., Results: IL-17 cytokines, particularly IL-17A, have been implicated in the development of various inflammatory and autoimmune disorders, including multiple sclerosis, Hashimoto's thyroiditis, systemic lupus erythematosus, pyoderma gangrenosum, autoimmune hepatic disorders, rheumatoid arthritis, psoriasis, psoriatic arthritis, ankylosing spondylitis, osteoarthritis, and graft- versus -host disease. Understanding the role of IL-17 in these diseases is crucial for developing targeted therapeutic strategies., Conclusion: The significant involvement of IL-17 cytokines in inflammatory and autoimmune diseases underscores their potential as therapeutic targets. Current treatments utilizing antibodies against IL-17 cytokines and IL-17RA receptors have shown promise in managing these conditions. This review consolidates the understanding of IL-17 family members and their roles, providing valuable insights for the development of novel immunomodulators to effectively treat inflammatory and autoimmune diseases., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Background and Aims: Necrotizing enterocolitis (NEC) is a life-threatening disease and the most common gastrointestinal emergency in premature infants. Accurate early diagnosis is challenging. Modified Bell's staging is routinely used to guide diagnosis, but early diagnostic signs are nonspecific, potentially leading to unobserved disease progression, which is problematic given the often rapid deterioration observed. We investigated fecal cytokine levels, coupled with gut microbiota profiles, as a noninvasive method to discover specific NEC-associated signatures that can be applied as potential diagnostic markers., Methods: Premature babies born below 32 weeks of gestation were admitted to the 2-site neonatal intensive care unit (NICU) of Imperial College hospitals (St. Mary's or Queen Charlotte's & Chelsea) between January 2011 and December 2012. During the NICU stay, expert neonatologists grouped individuals by modified Bell's staging (healthy, NEC1, NEC2/3) and fecal samples from diapers were collected consecutively. Microbiota profiles were assessed by 16S rRNA gene amplicon sequencing and cytokine concentrations were measured by V-Plex multiplex assays., Results: Early evaluation of microbiota profiles revealed only minor differences. However, at later time points, significant changes in microbiota composition were observed for Bacillota (adj. P  = .0396), with Enterococcus being the least abundant in Bell stage 2/3 NEC. Evaluation of fecal cytokine levels revealed significantly higher concentrations of IL-1α ( P  = .045), IL-5 ( P  = .0074), and IL-10 ( P  = .032) in Bell stage 1 NEC compared to healthy individuals., Conclusion: Differences in certain fecal cytokine profiles in patients with NEC indicate their potential use as diagnostic biomarkers to facilitate earlier diagnosis. Additionally, associations between microbial and cytokine profiles contribute to improving knowledge about NEC pathogenesis., (© 2023 The Authors.)

Despite a clear epidemiological link between autoimmune disease and cardiovascular (CV) risk exists, pathophysiological explanations are extremely complex and far from being elucidated. Dysregulation of metabolic pathways and chronic low-grade inflammation represent common pathways, but CV risk still remains underestimated in patients with autoimmune diseases. Among different candidate mediators, pro-protein convertase subtilisin/kexin type 9 (PCSK9) is attracting growing attention, due to a combined effect on lipid metabolism and inflammatory response. Studies on PCSK9 inhibitors have established a clear benefit on CV outcome without an established effect on inflammation. Conversely, evidence from sepsis and HIV infection strongly supports a pro-inflammatory role of PCSK9. Still, the role of PCSK9 in autoimmune diseases is uncertain. So far, reported clinical findings are controversial and likely reflect the poor knowledge of PCSK9 activity on monocyte/macrophage migration and activation. The complex signaling network around PCSK9 synthesis and metabolism may also have a role, especially concerning the involvement of scavenger receptors, such as CD36. Such complexity in PCSK9 signaling seems particularly evident in autoimmune disease model. This would also potentially explain the observed independency between lipid profile and PCSK9 levels, the so-called "lipid paradox". In this narrative review, we will summarize the current knowledge about the complex network of PCSK9 signaling. We will focus on upstream and downstream pathways with potential implication in autoimmune disease and potential effects of PCSK9 inhibiting strategies., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)