Figure 3
Figure 3. Th17 cells in GVHD. Th17 cells traffic to the lung and skin by CCR6, where they mediate tissue damage. In the lung, Th17 cells secrete IL-17A, IL-17F, and TNF, which induce secretion of proinflammatory cytokines and chemokines by epithelial cells. Th17-derived cytokines act directly on neutrophils (neut), resulting in production of matrix metalloproteinases (MMPs), reactive oxygen species (ROS), and TNF. In the skin, IL-17A and IL-17F produced by infiltrating Th17 cells cause the production of several proinflammatory cytokines and chemokines by keratinocytes, resulting in further leukocyte recruitment and local tissue damage. IL-22 is secreted byTh17 cells and possibly Th22 cells activated by Langerhan cells (LCs). IL-22 induces keratinocyte proliferation, resulting in acanthosis and cutaneous GVHD pathology.

Th17 cells in GVHD. Th17 cells traffic to the lung and skin by CCR6, where they mediate tissue damage. In the lung, Th17 cells secrete IL-17A, IL-17F, and TNF, which induce secretion of proinflammatory cytokines and chemokines by epithelial cells. Th17-derived cytokines act directly on neutrophils (neut), resulting in production of matrix metalloproteinases (MMPs), reactive oxygen species (ROS), and TNF. In the skin, IL-17A and IL-17F produced by infiltrating Th17 cells cause the production of several proinflammatory cytokines and chemokines by keratinocytes, resulting in further leukocyte recruitment and local tissue damage. IL-22 is secreted byTh17 cells and possibly Th22 cells activated by Langerhan cells (LCs). IL-22 induces keratinocyte proliferation, resulting in acanthosis and cutaneous GVHD pathology.

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