Fig. 1

Pattern diagram of the mechanisms of autoimmune diseases. After differentiation of hematopoietic stem cells, progenitor T cell (pro-T cell) will leave the bone marrow and enter the thymus, and differentiate from double-negative (DN) T cells into double-positive (DP) T cells. Under death by neglect, negative selection, and positive selection via thymic epithelial cells, single positive T cells with low avidity to autoantigens-MHC complexes survive and differentiate into CD4 or CD8 and enter the periphery. However, some autoreactive T cells can avoid these select clearance effects and enter the peripheral. These autoreactive T cells include three types: (1) molecular mimicry, TCR can recognize the autoantigens and foreign antigens similar to autoantigens such as viruses and some bacteria. (2) dual TCRs, one TCR can recognize the non-autoantigens and another can recognize the autoantigens. (3) chimeric TCR, different Vα and Vβ combinations can recognize the autoantigens and non-autoantigens. Viruses, bacteria, and other autoantigens lead to the necrosis of autologous cells and result in the release of autoantigens. Some bacteria similar to autoantigens can induce the activation of these T cells susceptible to autoantigens and promote the autoimmune disease. Besides, the stimulation of external antigens can promote the continuous inflammatory environment and lead to the highly activated immune state of T and B cells. These T cells can secrete various inflammatory cytokines, activate B cells and recruit many immune cells, and induce inflammatory reaction. Eventually this will lead to the occurrence and development of autoimmune diseases. (Part of the figure was modified from Servier Medical Art(http://smart.servier.com/), licensed under a Creative Common Attribution 4.0 Generic License. (https://creativecommons.org/licenses/by/4.0/)