7 results on '"Jiahui Zhang"'
Search Results
2. Utilizing murine dendritic cell line DC2.4 to evaluate the immunogenicity of subunit vaccines in vitro
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Lantian Lu, Wei Yang Kong, Jiahui Zhang, Farrhana Firdaus, James W. Wells, Rachel J. Stephenson, Istvan Toth, Mariusz Skwarczynski, and Jazmina L. Gonzalez Cruz
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DC2.4 ,dendritic cell uptake ,dendritic cell maturation ,in vitro assay ,subunit vaccine ,Immunologic diseases. Allergy ,RC581-607 - Abstract
Subunit vaccines hold substantial promise in controlling infectious diseases, due to their superior safety profile, specific immunogenicity, simplified manufacturing processes, and well-defined chemical compositions. One of the most important end-targets of vaccines is a subset of lymphocytes originating from the thymus, known as T cells, which possess the ability to mount an antigen-specific immune response. Furthermore, vaccines confer long-term immunity through the generation of memory T cell pools. Dendritic cells are essential for the activation of T cells and the induction of adaptive immunity, making them key for the in vitro evaluation of vaccine efficacy. Upon internalization by dendritic cells, vaccine-bearing antigens are processed, and suitable fragments are presented to T cells by major histocompatibility complex (MHC) molecules. In addition, DCs can secrete various cytokines to crosstalk with T cells to coordinate subsequent immune responses. Here, we generated an in vitro model using the immortalized murine dendritic cell line, DC2.4, to recapitulate the process of antigen uptake and DC maturation, measured as the elevation of CD40, MHC-II, CD80 and CD86 on the cell surface. The levels of key DC cytokines, tumor necrosis alpha (TNF-α) and interleukin-10 (IL-10) were measured to better define DC activation. This information served as a cost-effective and rapid proxy for assessing the antigen presentation efficacy of various vaccine formulations, demonstrating a strong correlation with previously published in vivo study outcomes. Hence, our assay enables the selection of the lead vaccine candidates based on DC activation capacity prior to in vivo animal studies.
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- 2024
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3. Risk factors of neuropathic pain in multiple sclerosis: a retrospective case-cohort study
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Huiying Ouyang, Xiaojun Li, Haoyou Xu, Yibo Zhan, Zequan Zheng, Guixian Chen, Zhenzhen Lou, Haoxuan Chen, Jiahui Zhang, Hui Mao, Changlin Zhang, Lulu Qin, Yuanqi Zhao, and Min Zhao
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spinal cord lesions ,basal ganglia ,multiple sclerosis ,neuropathic pain ,MRI ,Immunologic diseases. Allergy ,RC581-607 - Abstract
BackgroundPain is a common symptom in multiple sclerosis (MS), especially neuropathic pain, which has a significant impact on patients’ mental and physical health and quality of life. However, risk factors that related to neuropathic pain, still remain unclear.ObjectiveThe study aimed to explore the risk factors of neuropathic pain among MS patients.Materials and methodsThis retrospective study examined the consecutive patients diagnosed with MS in the Department of Neurology of Guangdong Provincial Hospital of Chinese Medicine between August 2011 and October 2022. Neuropathic pain was defined as “pain arising as a direct consequence of a lesion or disease affecting the somatosensory system”. Demographic and clinical features were obtained from the electronic system of the hospital.ResultsOur cohort revealed that the prevalence of patients with neuropathic pain in MS was 34.1%. The results indicated that the longer the spinal lesions, the greater the neuropathic pain risks (2-4: OR, 13.3(2.1-82), >5: OR, 15.2(2.7-86.8), p for tread: 0.037). Meanwhile, multivariate regression analysis showed that cervical and thoracic lesions (OR 4.276, 95% CI 1.366-13.382, P = 0.013), upper thoracic lesions (T1-T6) (OR 3.047, 95% CI 1.018-9.124, P = 0.046) were positively correlated with neuropathic pain, while basal ganglia lesions (OR 0.188, 95% CI 0.044-0.809, P = 0.025) were negatively correlated with neuropathic pain among MS patients.ConclusionExtended spinal lesions (≥3 spinal lesions), cervical and thoracic lesions, upper thoracic lesions were independent risk factors of neuropathic pain among MS patients. Furthermore, our study found that the longer the spinal lesions, the greater the neuropathic pain risks.
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- 2024
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4. MAPK8 and CAPN1 as potential biomarkers of intervertebral disc degeneration overlapping immune infiltration, autophagy, and ceRNA
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Yuxin Zhang, Jiahui Zhang, Zhongyi Sun, Hui Wang, Ruonan Ning, Longyu Xu, Yichen Zhao, Kai Yang, Xiaobing Xi, and Jiwei Tian
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intervertebral disc degeneration (IDD) ,immune infiltration ,bioinformatic analysis ,autophagy ,MAPK8 ,CAPN1 ,Immunologic diseases. Allergy ,RC581-607 - Abstract
BackgroundIntervertebral disc degeneration (IDD) is one of the most common health problems in the elderly and a major causative factor in low back pain (LBP). An increasing number of studies have shown that IDD is closely associated with autophagy and immune dysregulation. Therefore, the aim of this study was to identify autophagy-related biomarkers and gene regulatory networks in IDD and potential therapeutic targets.MethodsWe obtained the gene expression profiles of IDD by downloading the datasets GSE176205 and GSE167931 from the Gene Expression Omnibus (GEO) public database. Subsequently, differentially expressed genes (DEGs) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, gene ontology (GO), and gene set enrichment analysis (GSEA) were performed to explore the biological functions of DEGs. Differentially expressed autophagy-related genes (DE-ARGs) were then crossed with the autophagy gene database. The hub genes were screened using the DE-ARGs protein–protein interaction (PPI) network. The correlation between the hub genes and immune infiltration and the construction of the gene regulatory network of the hub genes were confirmed. Finally, quantitative PCR (qPCR) was used to validate the correlation of hub genes in a rat IDD model.ResultsWe obtained 636 DEGs enriched in the autophagy pathway. Our analysis revealed 30 DE-ARGs, of which six hub genes (MAPK8, CTSB, PRKCD, SNCA, CAPN1, and EGFR) were identified using the MCODE plugin. Immune cell infiltration analysis revealed that there was an increased proportion of CD8+ T cells and M0 macrophages in IDD, whereas CD4+ memory T cells, neutrophils, resting dendritic cells, follicular helper T cells, and monocytes were much less abundant. Subsequently, the competitive endogenous RNA (ceRNA) network was constructed using 15 long non-coding RNAs (lncRNAs) and 21 microRNAs (miRNAs). In quantitative PCR (qPCR) validation, two hub genes, MAPK8 and CAPN1, were shown to be consistent with the bioinformatic analysis results.ConclusionOur study identified MAPK8 and CAPN1 as key biomarkers of IDD. These key hub genes may be potential therapeutic targets for IDD.
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- 2023
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5. RIPK1-Associated Inborn Errors of Innate Immunity
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Jiahui Zhang, Taijie Jin, Ivona Aksentijevich, and Qing Zhou
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RIPK1 ,programmed cell death ,immunodeficiency ,autoinflammatory disease ,CRIA ,biological therapies ,Immunologic diseases. Allergy ,RC581-607 - Abstract
RIPK1 (receptor-interacting serine/threonine-protein kinase 1) is a key molecule for mediating apoptosis, necroptosis, and inflammatory pathways downstream of death receptors (DRs) and pattern recognition receptors (PRRs). RIPK1 functions are regulated by multiple post-translational modifications (PTMs), including ubiquitination, phosphorylation, and the caspase-8-mediated cleavage. Dysregulation of these modifications leads to an immune deficiency or a hyperinflammatory disease in humans. Over the last decades, numerous studies on the RIPK1 function in model organisms have provided insights into the molecular mechanisms of RIPK1 role in the maintenance of immune homeostasis. However, the physiological role of RIPK1 in the regulation of cell survival and cell death signaling in humans remained elusive. Recently, RIPK1 loss-of-function (LoF) mutations and cleavage-deficient mutations have been identified in humans. This review discusses the molecular pathogenesis of RIPK1-deficiency and cleavage-resistant RIPK1 induced autoinflammatory (CRIA) disorders and summarizes the clinical manifestations of respective diseases to help with the identification of new patients.
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- 2021
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6. CTLA-4 expression on CD4+ lymphocytes in patients with sepsis-associated immunosuppression and its relationship to mTOR mediated autophagic--lysosomal disorder.
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Wei Cheng, Jiahui Zhang, Dongkai Li, Xianli Lei, Hao Wang, and Na Cui
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MONONUCLEAR leukocytes ,T cells ,CYTOTOXIC T lymphocyte-associated molecule-4 ,LYSOSOMAL storage diseases ,REFERENCE values - Abstract
Background: The aim of this study was to clarify the relationship between expression level of CTLA-4 on CD4
+ T cells and sepsis-associated immunosuppression (SAI), and to elucidate the possible mechanism of mTOR pathwaymediated autophagic-lysosomal disorder in regulating CTLA-4 expression. Methods: We enrolled 63 sepsis patients admitted to our ICU between January 1 and June 30, 2023. Peripheral blood mononuclear cells were isolated from the patients within 24 hours of recruitment. Expression levels of mTOR, P62, LC3II, and CTLA-4 on circulating CD4+ T lymphocytes were quantitated using flow cytometry. The association of these markers and relationship between CTLA-4 expression and the incidence of SAI and 28-day mortality were comprehensively analyzed. Results: Compared with non-immunosuppressed patients with sepsis, patients with SAI had a higher 28-day mortality rate (37.5% vs 13.0%, P=0.039) and higher CTLA-4 mean fluorescence intensity (MFI) on CD4+ T cells (328.7 versus 78.7, P<0.0001). CTLA-4 MFI on CD4+ cells was independently associated with the occurrence of SAI (95% confidence interval: 1.00-1.14, P=0.044). In patients with sepsis and SAI, non-survivors had higher CTLA-4 expression than survivors (sepsis: 427.5 versus 130.6, P=0.002; and SAI: 506.7 versus 225.2, P<0.0001). The sensitivity and specificity of CTLA-4 MFI at predicting 28-day mortality in patients with SAI was 100% and 80% respectively with the cutoff value of 328.7 and the area under the curve of 0.949. The MFI of mTOR, P62, and LC3II on CD4+ T cells were statistically higher in patients with SAI than in nonimmunosuppressed patients (267.2 versus 115.9, P<0.0001; 314.8 versus 173.7, P<0.0001; and 184.7 versus 1123.5, P=0.012, respectively); P62 and LC3II were markedly higher in non-survivors than in survivors of sepsis (302.9 versus 208.9, P=0.039; and 244.3 versus 122.8, P<0.0001 respectively). The expression of CTLA-4 statistically correlated with that of LC3II in patients with sepsis, patients with SAI, and patients with SAI who did not survive (correlation coefficient: 0.69, 0.68, and 0.73, respectively, P<0.0001). Conclusions: CTLA-4 overexpression on CD4+ T cells was markedly associated with the incidence of SAI and had great relevance to 28-day mortality. mTOR pathway mediated autophagic-lysosomal disorder showed significant association with CTLA-4 expression. [ABSTRACT FROM AUTHOR]- Published
- 2024
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7. Effects of Neutrophil Extracellular Traps in Patients With Septic Coagulopathy and Their Interaction With Autophagy
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Jianwei Chen, Jia-Yu Mao, Wei Cheng, Jiahui Zhang, and Na Cui
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Male ,autophagy ,medicine.medical_specialty ,Immunology ,Inflammation ,Extracellular Traps ,Severity of Illness Index ,Gastroenterology ,sepsis ,Sepsis ,DIC ,Risk Factors ,Internal medicine ,Coagulopathy ,Humans ,Medicine ,Immunology and Allergy ,Prospective Studies ,septic coagulopathy ,Original Research ,Aged ,Aged, 80 and over ,Disseminated intravascular coagulation ,biology ,business.industry ,Area under the curve ,NETs ,Neutrophil extracellular traps ,RC581-607 ,Disseminated Intravascular Coagulation ,Middle Aged ,medicine.disease ,Immunity, Innate ,Logistic Models ,Neutrophil elastase ,biology.protein ,Biomarker (medicine) ,Female ,Immunologic diseases. Allergy ,medicine.symptom ,business ,Biomarkers - Abstract
IntroductionNeutrophil extracellular traps (NETs) act as a critical trigger of inflammation and coagulation. We hypothesized that NETs are associated with septic hypercoagulability.Materials and MethodsIn total, 82 patients admitted with sepsis in the Department of Critical Care Medicine of Peking Union Medical College Hospital were enrolled between February 2017 and April 2018. Clinical and hematological parameters and thrombotic or hemorrhagic events were recorded. Blood samples were obtained to assess biomarkers of NET formation, including neutrophil elastase 2 (ELA2) and citrullinated histone H3, and endothelial-derived biomarker syndecan-1. Autophagy levels and their regulation pathway were also examined to explore their interaction with NETs.ResultSepsis patients with disseminated intravascular coagulation (DIC) showed significantly higher levels of NET formation [ELA2, 1,247 (86–625) vs. 2,039 (1,544–2,534), p < 0.0001; H3, 140 (47–233) vs. 307 (199–415), p < 0.0001]. NET formation was independently associated with DIC risk [ELA2, OR 1.0028, 95% CI, 1.0010–1.0045; H3, OR 1.0104, 95% CI, 1.0032–1.0176] and mortality [ELA2, HR 1.0014, 95% CI, 1.0004–1.0024; H3, HR 1.0056, 95% CI, 1.0008–1.0115]. The area under the curve value for ELA2 in predicting DIC occurrence was 0.902 (95% CI, 0.816–0.957), and that of H3 was 0.870 (95% CI, 0.778–0.934). Furthermore, biomarkers of NET formation, endothelial cells, and autophagy exhibited a significant correlation [ELA2 and Syn (r = 0.5985, p < 0.0001), LC3B (r = −0.4224, p < 0.0001); H3 and Syn (r = 0.6383, p < 0.0001), LC3B (r = −0.3005, p = 0.0061)].ConclusionIncreased NET formation is significantly associated with sepsis-induced DIC incidence and mortality in sepsis patients, revealing a significant relationship with the autophagy pathway.Clinical Trial Registrationchictr.org.cn, identifier ChiCTR-ROC-17010750.
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- 2021
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