Scientists have found that activation of non-regulatory antigen-presenting cells by T cells can destroy autoimmune tolerance

Scientists have found that activation of non-regulatory antigen-presenting cells by T cells can destroy autoimmune tolerance

February 02, 2019 Source: Ministry of Science and Technology

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On January 15th, researchers from Pohang University of Science and Technology in South Korea and the University of New South Wales in Australia published an article entitled “Unregulated antigen-presenting cell activation by T cells breaks self tolerance” on PNAS, and found that T cells caused non-regulation. Activation of sex antigen presenting cells can destroy autoimmune tolerance.

Removal of a subset of regulatory T cells (Tregs) can impair the body's immune homeostasis and lead to T cell proliferation and autoimmune diseases. In the present study, the researchers found that in the case of CD4+ Foxp3+ T regulatory cells [natural regulatory T cells (nTregs)] acute depletion, or the transfer of naive T cells into nTregs immunodeficient Rag1?/? mice, mice Self-T cells proliferate rapidly. In mice cultured in an antigen-free (AF) environment, in both cases T cell proliferation is directed against autoantigens and not against food or foreign antigens. In vivo studies have shown that deletion of nTregs increases expression of mouse dendritic cells (DCs) B7 and allows a small fraction of highly self-affinitive primary CD4 T cells to respond significantly to host DCs, ie T/DC Bidirectional interactions result in DC activation and T cell proliferation, accompanied by the formation of peripheral Treg (pTreg). Similarly, high-affinity CD4 T cells cultured in the presence of autologous DCs in vitro without nTregs also proliferate and form pTregs, an autoimmune response that is MHCII/peptide-dependent, from cultured dendritic cells B7. Increased by the level. This study provides data support for the self-tolerance model regulated by CD28 signaling and explains the pathological effects of CD28 superantibodies.

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