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. 2016 Aug 11;17(8):1288. doi: 10.3390/ijms17081288

Figure 1.

Figure 1

Schematic graph of GVHD initiated by intestinal flora. Intestinal flora enter the systemic circulation through damaged intestinal mucosa, and then interact with Toll-like receptors (TLRs), leading to the upregulation of major histocompatibility complex class II (MHCII) and costimulatory molecules B7 on host APCs. The upregulation of MHCII and costimulatory molecules B7 present the first and second activation signals, respectively, to donor T cells for the production of cytokines (including IL-1, IL-6, IL-12, IL-21, IL-22, IL-23, TNF-α and IFN-γ). The cytokines then induce the differentiation of a sub-population of donor T cells (Th1/Th2). Subsequently, the activated donor-derived T cells attack target tissues or organs (including intestine, liver and skin) by direct cytotoxicity, and eventually leading to GVHD. PAMPs = pathogen-associated molecular patterns; APCs = antigen-presenting cells; Th1 = helper T cell 1; Th2 = helper T cell 2.