OX40, a member of the TNF receptor family, is primarily recognized for its role in promoting effector T cell differentiation, proliferation, long-term survival, and the production of pro-inflammatory cytokines. It also inhibits the differentiation and suppressive activity of regulatory T cells (Tregs). OX40 is expressed on activated CD4+ and CD8+ T cells, as well as on other cell types. The OX40 ligand, expressed by antigen-presenting cells (APCs), activates the OX40 signaling pathway, which enhances the immune response. The interaction between OX40 and its ligand leads to increased CD4+ and CD8+ cell proliferation, stimulated cytokine production, and improved survival of antigen-specific memory T cells. OX40 expression has been identified as an unfavorable prognostic marker and may be a potential target for future immunotherapies. In the context of esophageal carcinoma (EC), OX40 has been identified as a novel molecule; its elevated expression is associated with favorable clinical outcomes. As a second immune checkpoint, OX40 may have significant implications for the prognosis and immunomodulation of EC patients. In mice, the absence of OX40 results in a significant reduction in the number of effector memory CD4+ cells and a diminished CD8+ response, leading to accelerated tumor growth. Consequently, the immune-stimulating properties of OX40 agonists could potentially counteract some of the immunosuppressive properties within the tumor environment.
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