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. 2021 Feb 26;12:597761. doi: 10.3389/fimmu.2021.597761

Figure 1.

Figure 1

Immunoregulatory molecules and cytokines implicated in Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN). CD8+ cytotoxic T lymphocytes (CTLs) play a central role in the pathogenesis of SJS/TEN. Cytokines (including IL-15 and TNF) and costimulatory molecules of APCs can stimulate the CTLs, which in turn produce cytokines, including IFN-γ and IL-15. CTL and NK cell degranulation that induce keratinocyte apoptosis may be mediated, at least partially, by the interaction between CD49/NKG2C and HLA-E. Other players in SJS/TEN include Fas/FasL interactions, T cells and keratinocytes expressing PD-L1, and CD40/CD40L interactions at the dermal-epidermal junction. Ag, antigen; APC, antigen presenting cell; CD40(L), cluster of differentiation 40 (ligand); FasL, Fas ligand; GNLY, granulysin; GzmB, granzyme B; HLA-E, HLA class I histocompatibility antigen, alpha chain E; IFN-γ, interferon gamma; IL-15, Interleukin 15; MHC, major histocompatibility complex; NK cell, natural killer cell; Perf, perforin; PD-L1, programmed death ligand-1; TCR, T cell receptor; TNF, tumor necrosis factor; Treg: regulatory T cell.