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The phrase Effector T cells and APCs via Treg-derived immunosuppressive cytokines refers to a primary mechanism of immune suppression where Regulatory T cells (Tregs) secrete inhibitory signaling molecules to dampen immune activity. The key cytokines involved in this process are Interleukin-10 (IL-10), Transforming Growth Factor-beta (TGF-beta), and Interleukin-35 (IL-35) (Vignali et al., 2008, Nature Reviews Immunology). These cytokines act on Effector T cells (Teffs) to block their proliferation and cytokine production, and on Antigen-Presenting Cells (APCs) to reduce their ability to activate new T cells by downregulating MHC and co-stimulatory molecules (Shevach, 2009, Immunity). In oncology, tumors often exploit this pathway to create an immunosuppressive microenvironment that evades the host immune system, making these cytokines major targets for checkpoint inhibition and combination therapies (Facciabene et al., 2012, Cancer Research). Conversely, in autoimmune disorders, therapeutic efforts focus on enhancing this suppressive axis to restore self-tolerance and prevent tissue damage (Sakaguchi et al., 2008, Cell).
Modulation of the immune system by either inhibiting these cytokines to enhance anti-tumor responses or administering/inducing them to suppress autoimmune and inflammatory reactions.
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