Abstract
T Follicular helper (Tfh) cells, a unique subset of CD4+ T cells, play an essential role in B cell development and the formation of germinal centers (GCs). Tfh differentiation depends on various factors including cytokines, transcription factors and multiple costimulatory molecules. Given that OX40 signaling is critical for costimulating T cell activation and function, its roles in regulating Tfh cells have attracted widespread attention. Recent data have shown that OX40/OX40L signaling can not only promote Tfh cell differentiation and maintain cell survival, but also enhance the helper function of Tfh for B cells. Moreover, upregulated OX40 signaling is related to abnormal Tfh activity that causes autoimmune diseases. This review describes the roles of OX40/OX40L in Tfh biology, including the mechanisms by which OX40 signaling regulates Tfh cell differentiation and functions, and their close relationship with autoimmune diseases.
Highlights
Many autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are characterized by autoantibody production
Adam L et al found that OX40 and ICOS were coexpressed on peripheral blood T Follicular helper (Tfh) cells of patients with primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC)
We have found that OX40/OX40L was abnormally and persistently coexpressed on CD4+ T cells from Graves’ disease (GD) patients, and the coexpression level was closely related to TRAb [117]
Summary
Many autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are characterized by autoantibody production. A specialized cell subset named T follicular helper (Tfh) cells has attract much attention because of their requirement for B cell help and the production of high affinity class-switched antibodies. Tfh cells, located in lymphoid follicles, belong to a distinct CD4+ T subset. They are essential for generation of effective and long-lived humoral immune responses. Several pairs of costimulatory molecules have been demonstrated to control Tfh development and function. OX40 and OX40L play a critical role in enhancement of immune responses and participate in the development of autoimmune diseases. It was reported that the OX40/OX40L interaction is required for the functions of Tfh cells. This article focuses on the effects of OX40/OX40L signaling on Tfh cells and their roles in the pathogenesis of autoimmune diseases
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