T follicular helper cells and T follicular regulatory cells in autoimmune diseases

Qi, Juntong; Liu, Chang; Bai, Ziran; Li, Xia; Yao, Genhong

doi:10.3389/fimmu.2023.1178792

Cited by 18 publications

(8 citation statements)

References 155 publications

(128 reference statements)

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“…In addition, COVID-19 convalescent patients showed a negative correlation between levels of circulating Tfr cells and serum virus-specific IgM, IgG, and IgA antibodies. Follicular Treg cells may potentially play an important role in controlling humoral memory response and antibody specificity, as well as preventing auto-antibody formation [ 83 ].…”

Section: Resultsmentioning

confidence: 99%

Tuberculosis and COVID-19 Dually Affect Human Th17 Cell Immune Response

et al. 2023

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COVID-19 infection not only profoundly impacts the detection of tuberculosis infection (Tbc) but also affects modality in tuberculosis patient immune response. It is important to determine immune response alterations in latent tuberculosis infection as well as in SARS-CoV-2-infected tuberculosis patients. Such changes may have underlying effects on the development and course of further tuberculosis. Here, we aimed to review the characteristics of immune response in TB patients or convalescent COVID-19 patients with latent TB infection (LTBI). Materials and Methods. We analyzed the features of immune response in tuberculosis and COVID-19 patients. For this, we analyzed publications released from December 2019 to March 2023; those which were published in accessible international databases (“Medline”, “PubMed”, “Scopus”) and with keywords such as “COVID-19”, “SARS-CoV-2”, “tuberculosis”, “pulmonary tuberculosis”, “latent tuberculosis infection”, “Treg”, “follicular Treg”, and “Treg subsets”, we considered. Results. Through our analysis, we found that tuberculosis patients who had been infected with COVID-19 previously and elevated Th1 and Th2 cell levels. High levels of Th1 and Th2 cells may serve as a positive marker, characterizing activated immune response during TB infection. COVID-19 or post-COVID-19 subjects showed decreased Th17 levels, indicating a lack of tuberculosis development. Moreover, the typical course of tuberculosis is associated with an increase in Treg level, but COVID-19 contributes to a hyperinflammatory response. Conclusion. According to the data obtained, the course of tuberculosis proceeds in a dissimilar way due to the distinct immune response, elicited by SARS-CoV-2. Importantly, the development of active tuberculosis with a severe course is associated with a decline in Treg levels. Both pathogens lead to disturbed immune responses, increasing the risk of developing severe TB. The insights and findings of this paper may be used to improve the future management of individuals with latent and active tuberculosis.

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Section: Resultsmentioning

confidence: 99%

Tuberculosis and COVID-19 Dually Affect Human Th17 Cell Immune Response

et al. 2023

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“…The abnormal number or function of Tfh plays a crucial role in the development of autoimmune disorders such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). (Qi et al, 2023). This may indicate that EM may be closely related to autoimmune diseases.…”

Section: Discussionmentioning

confidence: 97%

Construction and evaluation of endometriosis diagnostic prediction model and immune infiltration based on efferocytosis-related genes

Pei,

Jia,

Lin

et al. 2024

Front. Mol. Biosci.

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Background: Endometriosis (EM) is a long-lasting inflammatory disease that is difficult to treat and prevent. Existing research indicates the significance of immune infiltration in the progression of EM. Efferocytosis has an important immunomodulatory function. However, research on the identification and clinical significance of efferocytosis-related genes (EFRGs) in EM is sparse.Methods: The EFRDEGs (differentially expressed efferocytosis-related genes) linked to datasets associated with endometriosis were thoroughly examined utilizing the Gene Expression Omnibus (GEO) and GeneCards databases. The construction of the protein-protein interaction (PPI) and transcription factor (TF) regulatory network of EFRDEGs ensued. Subsequently, machine learning techniques including Univariate logistic regression, LASSO, and SVM classification were applied to filter and pinpoint diagnostic biomarkers. To establish and assess the diagnostic model, ROC analysis, multivariate regression analysis, nomogram, and calibration curve were employed. The CIBERSORT algorithm and single-cell RNA sequencing (scRNA-seq) were employed to explore immune cell infiltration, while the Comparative Toxicogenomics Database (CTD) was utilized for the identification of potential therapeutic drugs for endometriosis. Finally, immunohistochemistry (IHC) and reverse transcription quantitative polymerase chain reaction (RT-qPCR) were utilized to quantify the expression levels of biomarkers in clinical samples of endometriosis.Results: Our findings revealed 13 EFRDEGs associated with EM, and the LASSO and SVM regression model identified six hub genes (ARG2, GAS6, C3, PROS1, CLU, and FGL2). Among these, ARG2, GAS6, and C3 were confirmed as diagnostic biomarkers through multivariate logistic regression analysis. The ROC curve analysis of GSE37837 (AUC = 0.627) and GSE6374 (AUC = 0.635), along with calibration and DCA curve assessments, demonstrated that the nomogram built on these three biomarkers exhibited a commendable predictive capacity for the disease. Notably, the ratio of nine immune cell types exhibited significant differences between eutopic and ectopic endometrial samples, with scRNA-seq highlighting M0 Macrophages, Fibroblasts, and CD8 Tex cells as the cell populations undergoing the most substantial changes in the three biomarkers. Additionally, our study predicted seven potential medications for EM. Finally, the expression levels of the three biomarkers in clinical samples were validated through RT-qPCR and IHC, consistently aligning with the results obtained from the public database.Conclusion: we identified three biomarkers and constructed a diagnostic model for EM in this study, these findings provide valuable insights for subsequent mechanistic research and clinical applications in the field of endometriosis.

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“…Previously, Tfh cells in the germinal center of secondary lymphoid organs were regarded as particularly effective at promoting B-cell responses in autoimmune diseases, including RA. 11,26,27 Subsequently, extrafollicular CD4 + T cells, termed Tph cells, were reported to play an important role in helping B cells within peripheral inflamed sites in patients with RA. 12,13 F I G U R E 4 CD4 + PD-1 + Foxp3 − T cells from patients with RA exhibited type 2 helper T-cell characteristics.…”

Section: Discussionmentioning

confidence: 99%

Pathologically expanded peripheral CD4⁺PD‐1⁺Foxp3⁻ T‐cell subset promotes B‐cell hyperactivity in patients with rheumatoid arthritis

Bai,

Liu,

Liu

et al. 2024

Rheumatology & Autoimmunity

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BackgroundRheumatoid arthritis (RA) is an autoimmune disease characterized by destructive polyarthritis, and abnormal T–B‐cell interactions may contribute to its pathogenesis. This study aimed to investigate the characteristics and roles of CD4+ programmed death 1 (PD‐1)+Foxp3− T cells in relation to the B‐cell response in patients with RA.MethodsThis study included 155 patients with RA and 36 age‐ and sex‐matched healthy controls (HCs) from the Second Hospital of Dalian Medical University in China. Flow cytometry was used to assess the proportion and properties of peripheral CD4+PD‐1+Foxp3+ T cells, including their proliferation, activation, cytokine production, and capacity to induce B‐cell differentiation.ResultsThe proportion of CD4+PD‐1+Foxp3− T cells was increased in patients with RA compared with HCs ([10.78 ± 0.60]% vs. [5.67 ± 0.40]%, p < 0.001), and this was positively associated with the B‐cell response. Compared with CD4+PD‐1+Foxp3+ T cells, CD4+PD‐1+Foxp3− T cells from patients with RA exhibited increased expression of Ki67 ([6.52 ± 0.41]% vs. [3.87 ± 0.42]%, p < 0.01) and activation markers, produced higher levels of cytokines, and showed enhanced B‐cell differentiation. Furthermore, anti‐interleukin‐6R antagonists decreased the proportion, activation, and cytokine production of CD4+PD‐1+Foxp3− T cells in vitro. The frequency of type 2 CD4+PD‐1+Foxp3− T cells was significantly higher in patients with RA than that in HCs ([37.27 ± 1.43]% vs. [29.05 ± 1.30]%, p < 0.05).ConclusionsPeripherally expanded CD4+PD‐1+Foxp3− T cells in patients with RA, which induced B‐cell hyperactivity, may be inclined toward type 2 helper T cells. Our findings revealed a novel T‐cell subset that contributes to B‐cell hyperactivity in the pathogenesis of RA.

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T follicular helper cells and T follicular regulatory cells in autoimmune diseases

Cited by 18 publications

References 155 publications

Tuberculosis and COVID-19 Dually Affect Human Th17 Cell Immune Response

Tuberculosis and COVID-19 Dually Affect Human Th17 Cell Immune Response

Construction and evaluation of endometriosis diagnostic prediction model and immune infiltration based on efferocytosis-related genes

Pathologically expanded peripheral CD4⁺PD‐1⁺Foxp3⁻ T‐cell subset promotes B‐cell hyperactivity in patients with rheumatoid arthritis

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T follicular helper cells and T follicular regulatory cells in autoimmune diseases

Cited by 18 publications

References 155 publications

Tuberculosis and COVID-19 Dually Affect Human Th17 Cell Immune Response

Tuberculosis and COVID-19 Dually Affect Human Th17 Cell Immune Response

Construction and evaluation of endometriosis diagnostic prediction model and immune infiltration based on efferocytosis-related genes

Pathologically expanded peripheral CD4+PD‐1+Foxp3− T‐cell subset promotes B‐cell hyperactivity in patients with rheumatoid arthritis

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Pathologically expanded peripheral CD4⁺PD‐1⁺Foxp3⁻ T‐cell subset promotes B‐cell hyperactivity in patients with rheumatoid arthritis