Mechanism of Follicular Helper T Cell Differentiation Regulated by Transcription Factors.
Long-Shan JiXue-Hua SunXin ZhangZhen-Hua ZhouZhuo YuXiao-Jun ZhuLing-Ying HuangMiao FangYa-Ting GaoMan LiYue-Qiu GaoPublished in: Journal of immunology research (2020)
Helping B cells and antibody responses is a major function of CD4+T helper cells. Follicular helper T (Tfh) cells are identified as a subset of CD4+T helper cells, which is specialized in helping B cells in the germinal center reaction. Tfh cells express high levels of CXCR5, PD-1, IL-21, and other characteristic markers. Accumulating evidence has demonstrated that the dysregulation of Tfh cells is involved in infectious, inflammatory, and autoimmune diseases, including lymphocytic choriomeningitis virus (LCMV) infection, inflammatory bowel disease (IBD), systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), IgG4-related disease (IgG4-RD), Sjögren syndrome (SS), and type 1 diabetes (T1D). Activation of subset-specific transcription factors is the essential step for Tfh cell differentiation. The differentiation of Tfh cells is regulated by a complicated network of transcription factors, including positive factors (Bcl6, ATF-3, Batf, IRF4, c-Maf, and so on) and negative factors (Blimp-1, STAT5, IRF8, Bach2, and so on). The current knowledge underlying the molecular mechanisms of Tfh cell differentiation at the transcriptional level is summarized in this paper, which will provide many perspectives to explore the pathogenesis and treatment of the relevant immune diseases.
Keyphrases
- induced apoptosis
- cell cycle arrest
- transcription factor
- systemic lupus erythematosus
- rheumatoid arthritis
- type diabetes
- dendritic cells
- disease activity
- healthcare
- gene expression
- adipose tissue
- palliative care
- cell proliferation
- skeletal muscle
- weight loss
- smoking cessation
- glycemic control
- heat stress
- dna binding
- network analysis