Mechanism of Follicular Helper T Cell Differentiation Regulated by Transcription Factors

Ji, Long-Shan; Sun, Xuehua; Zhang, Xin; Zhou, Zhenhua; Yu, Zhuo; Huang, Lingying; Fang, Miao; Gao, Yating; Li, Man; Gao, Yueqiu

doi:10.1155/2020/1826587

Cited by 37 publications

(25 citation statements)

References 68 publications

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“…Our gene expression data suggest that these antigen experienced T cells consist of memory Treg cells and/or Tfh cells. However, further evidence for a contribution of Tfh cells in the cHL TME is lacking in literature and characteristic markers like BCL-6 and CXCR5 30 , 31 are not present in our differentially expressed gene set. In addition, although Tfh cell markers CD200 and PD-1 are expressed at higher levels, the intensity of staining for those markers is usually lower in CD4+CD26- T cells in the HL TME compared to CD4+ T cells in germinal centers within the same tissue.…”

Section: Discussionmentioning

confidence: 83%

CD4+ T cells in classical Hodgkin lymphoma express exhaustion associated transcription factors TOX and TOX2

et al. 2022

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In classical Hodgkin lymphoma (cHL), the highly abundant CD4+ T cells in the vicinity of tumor cells are considered essential for tumor cell survival, but are ill-defined. Although they are activated, they consistently lack expression of activation marker CD26. In this study, we compared sorted CD4+CD26- and CD4+CD26+ T cells from cHL lymph node cell suspensions by RNA sequencing and T cell receptor variable gene segment usage analysis. This revealed that although CD4+CD26- T cells are antigen experienced, they have not clonally expanded. This may well be explained by the expression of exhaustion associated transcription factors TOX and TOX2 , immune checkpoints PDCD1 and CD200 , and chemokine CXCL13 , which were amongst the 100 significantly enriched genes in comparison with the CD4+CD26+ T cells. Findings were validated in single-cell RNA sequencing data from an independent cohort. Interestingly, immunohistochemistry revealed predominant and high frequency of staining for TOX and TOX2 in the T cells attached to the tumor cells. In conclusion, the dominant CD4+CD26- T cell population in cHL is antigen experienced, polyclonal, and exhausted. This population is likely a main contributor to the very high response rates to immune checkpoint inhibitors in cHL.

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Section: Discussionmentioning

confidence: 83%

CD4+ T cells in classical Hodgkin lymphoma express exhaustion associated transcription factors TOX and TOX2

et al. 2022

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“…and negative factors (Blimp-1, STAT5, IRF8, Bach2, etc.) [ 147 , 148 ]. On the other hand, Tfr is a type of cell in the Treg subgroup, which can inhibit the reaction in GC and the production of high-affinity antibody.…”

Section: Regulatory Effect Of Mscs On T Cells In Ramentioning

confidence: 99%

Regulatory Effect of Mesenchymal Stem Cells on T Cell Phenotypes in Autoimmune Diseases

Wei

Yuan

Wang

et al. 2021

Stem Cells International

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Research on mesenchymal stem cells (MSCs) starts from the earliest assumption that cells derived from the bone marrow have the ability to repair tissues. Several scientists have since documented the crucial role of bone marrow-derived MSCs (BM-MSCs) in processes such as embryonic bone and cartilage formation, adult fracture and tissue repair, and immunomodulatory activities in therapeutic applications. In addition to BM-MSCs, several sources of MSCs have been reported to possess tissue repair and immunoregulatory abilities, making them potential treatment options for many diseases. Therefore, the therapeutic potential of MSCs in various diseases including autoimmune conditions has been explored. In addition to an imbalance of T cell subsets in most patients with autoimmune diseases, they also exhibit complex disease manifestations, overlapping symptoms among diseases, and difficult treatment. MSCs can regulate T cell subsets to restore their immune homeostasis toward disease resolution in autoimmune conditions. This review summarizes the role of MSCs in relieving autoimmune diseases via the regulation of T cell phenotypes.

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“…STAT1, STAT3, and STAT4 can promote Tfh cell development. The deficiency of these STATs led to the reduction of Tfh cells [ 48 – 50 ]. In contrast, STAT5 plays a negative role in Tfh cell development and humoral immunity.…”

Section: T Follicular Helper (Tfh) Cell Differentiationmentioning

confidence: 99%

The Role of T Follicular Helper Cells and Interleukin-21 in the Pathogenesis of Inflammatory Bowel Disease

Sun

Kong

et al. 2021

Gastroenterology Research and Practice

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T follicular helper (Tfh) cells represent a novel subset of CD4+ T cells which can provide critical help for germinal center (GC) formation and antibody production. The Tfh cells are characterized by the expression of CXC chemokine receptor 5 (CXCR5), programmed death 1 (PD-1), inducible costimulatory molecule (ICOS), B cell lymphoma 6 (BCL-6), and the secretion of interleukin-21 (IL-21). Given the important role of Tfh cells in B cell activation and high-affinity antibody production, Tfh cells are involved in the pathogenesis of many human diseases. Inflammatory bowel disease (IBD) is a group of chronic inflammatory diseases characterized by symptoms such as diarrhea, abdominal pain, and weight loss. Ulcerative colitis (UC) and Crohn’s disease (CD) are the most studied types of IBD. Dysregulated mucosal immune response plays an important role in the pathogenesis of IBD. In recent years, many studies have identified the critical role of Tfh cells and IL-21 in the pathogenic process IBD. In this paper, we will discuss the role of Tfh cells and IL-21 in IBD pathogenesis.

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Mechanism of Follicular Helper T Cell Differentiation Regulated by Transcription Factors

Cited by 37 publications

References 68 publications

CD4+ T cells in classical Hodgkin lymphoma express exhaustion associated transcription factors TOX and TOX2

CD4+ T cells in classical Hodgkin lymphoma express exhaustion associated transcription factors TOX and TOX2

Regulatory Effect of Mesenchymal Stem Cells on T Cell Phenotypes in Autoimmune Diseases

The Role of T Follicular Helper Cells and Interleukin-21 in the Pathogenesis of Inflammatory Bowel Disease

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