Abstract
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.
Highlights
T follicular helper (Tfh) cells are a specialized subset of T helper (Th) cells that can migrate into germinal center (GC) and help B cells to differentiate into antibodyproducing plasma B cells and generate high-affinity antibodies [1]
Tfh cells play a central role in B cell activation and high-affinity antibody production; the dysfunction of Tfh may lead to allergic reactions, systemic autoimmune diseases, and chronic inflammation [3, 4]
In recent years, increasing evidence has implicated that Tfh cells and the related cytokine IL-21 participate in the pathogenesis of Inflammatory bowel disease (IBD)
Summary
T follicular helper (Tfh) cells are a specialized subset of T helper (Th) cells that can migrate into germinal center (GC) and help B cells to differentiate into antibodyproducing plasma B cells and generate high-affinity antibodies [1]. The generation of neutralizing antibodies by B lymphocytes is a critical step in immune response to viral or bacterial infections, which is one of the two types of adoptive immunity. This process needs direct crosstalk between activated B and T cells. The germinal center (GC) formation is critical in the generation of high-affinity antibodies and long-lived plasma cells, which is the base of humoral immune responses against pathogen infection. Tfh cell differentiation is regulated by various factors such as extracellular cytokines, cell-surface molecule interactions, multiple transcription factors, and microRNAs [25, 26]
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