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Systemic Lupus Erythematosus
Published in Jason Liebowitz, Philip Seo, David Hellmann, Michael Zeide, Clinical Innovation in Rheumatology, 2023
Vaneet K. Sandhu, Neha V. Chiruvolu, Daniel J. Wallace
Basic understanding of the role of T cells in autoimmunity is sufficient to understand their impact in SLE. T cells may lose self-tolerance either in the thymus or peripherally. There is evidence of abnormal T cell signaling that can be induced by serum IgG. In addition, T cells in SLE may express the CD40 ligand longer than in control groups after activation. These active T cells are usually either Th17 or follicular helper T cells, which produce lower amounts of IL-2 and increased IL-21, thus inducing B cell differentiation.33
Peripheral T-Cell Lymphoma
Published in Wojciech Gorczyca, Atlas of Differential Diagnosis in Neoplastic Hematopathology, 2014
Tumor cells are considered to arise from follicular helper T cells (Tfh). Laurent et al. [43] proposed that the derivation of T cells from TFH can be established when at least three TFH markers are expressed. f-PTCL shares some clinical, phenotypic, and morphologic features with AITL, which suggest that both disorders belong to the same disease spectrum. Both tumors originate from TFH with immunohistochemical expression of CD10, BCL6, PD-1, CCR5, SAP, and CXCL13. Miyoshi et al. [45] showed no significant differences between f-PTCL and AITL in clinicopathological features, confirming that f-PTCL may represent a peculiar stage of AITL. The similarities between AITL and f-PTCL were also reported by Bacon et al., Huang et al., and Qubaja et al. [36,38,40]. Presence of distinct recurrent chromosomal translocation t(5;9)(q33;q22) in the subset of f-PTCLs (~20%), however, may suggest that at least a subset of f-PTCLs is distinct from AITL [36,37,46]. The t(5;9) translocation was not reported in AITL. Future studies including gene expression programming (GEP), microRNA (miRNA) profiling, and next-generation sequencing will determine if f-PTCL constitutes separate entity or belongs to either PTCL or AITL category [44].
Paeoniflorin improves autoimmune myocarditis in young rat by inhibiting CXCR5 to reduce follicular helper T cells
Published in Autoimmunity, 2022
Chunxiao Wang, Lanlan Wang, Li Wang
The activation of B cells requires the assistance of CD4 + T cells [2]. Now, it is generally believed that the CD4 + T cell subsets of these helper B cells are a group of helper T cells. Follicular helper T cells (Tfh) remain in lymphoid follicles due to the high expression of CXCR5 [3]. Follicular helper T cells (Tfh) are a unique subset of CD4 + T lymphocytes, which play a special role in B cell help and antibody response regulation [4]. Tfh has cell surface receptors Programmed cell death-1 (PD-1) and CXCR5, and expresses Inducible T cell CO-Stimulator (ICOS), transcription factor Bcl-6, and cytokine IL-21. Tfh cells help B cells differentiate into plasma cells and stimulate the formation of germinal centers (GC) [5]. Previous study has shown that the balance of Tfh cells is disturbed in the pathological process of autoimmune myocarditis [6]. Tfh cell imbalance is related to the occurrence of an amount kinds of diseases, including autoimmune diseases, immune deficiencies, infectious diseases, tumors, and so on [5,7–9]. CD4 + T cells differentiate into Tfh cells and Th1 cells, which act as helper B cells and CD8 + T cells, respectively.
PADI4 (rs2240340), PDCD1 (rs10204525), and CTLA4 (231775) gene polymorphisms and polyarticular juvenile idiopathic arthritis
Published in British Journal of Biomedical Science, 2020
MA Ali, A Abdelaziz, M Ali, A Abonar, M Hanafy, H Hussein, H Shabana, R Abd El-Hmid, S Kaddafy
Secondly, we found that PDCD1 SNP rs10204525 is also strongly linked to JIA in genotypic, dominant and allelic models. Although there was no link with disease activity, there were strong links between genotypes and anti-CCP antibodies, RF and CHAQ score. This fails to support the report of Tejeda et al on North Europeans who found no link between this SNP and JIA [29]. PDCD1 rs10204525 is not a risk variant for type 1 diabetes mellitus development in two different studies [30,31]. Pathophysiology suggests a link between PDCD1 rs10204525 mutant homogenous TT genotype with higher PD-1+T cells than heterogeneous CT or wild homogenous CC genotypes [15,16]. PDCD1 gene encodes PD-1 protein, PD-1 is an immunosuppressive molecule expressed on T cell [12]. Along with its inhibitory function, the expression of PD-1 on T cells should be decreased in patients with JIA. This suggests that risk TT and, in turn, its associated increased expression of PD-1+T cells appears controversial to its function. However, there is also evidence suggesting that PD-1 expressed on follicular helper T cells (a subset of CD4+T cells) contributes to B-cell activation, and promoting antibody production [32]. Therefore, we speculate that in addition to its function as an inhibitory costimulatory molecule, PD-1 might have other effects in JIA.
Donor-specific anti-HLA antibodies by solid phase immunoassays: advantages and technical concerns
Published in International Reviews of Immunology, 2019
Pernille Koefoed-Nielsen, Bjarne Kuno Møller
Follicular helper T cells (Tfh) are essential for providing signals for B-cell proliferation and production of high-affinity antibodies, such as anti-HLA DSA. Recently, Désy et al. demonstrated that human allogeneic DCs stimulated with antibodies against HLA cl. II antigens preferentially differentiate human naive CD4+ T cells into Tfh cells.38 Kidney transplant recipients with anti-HLA cl. II DSA presented higher blood counts of circulating Tfh cells than those with anti-HLA cl. I DSAs. The authors suggest that alloantibodies against HLA cl. II after contact with allogenic DCs promote the differentiation of naive T cells to Tfh cells that, in turn, may facilitate broader and intensified immunization.