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. 2017 Nov 20;14(12):1020–1022. doi: 10.1038/cmi.2017.124

Figure 1.

Figure 1

Increased IL-17 induced by rituximab or irradiation promotes the growth of DLBCL cells. Anti-CD20 monoclonal antibody (rituximab) or irradiation promotes DLBCL cells to secrete IL-6, thereby inducing the secretion of IL-17 by Foxp3+Treg cells. This group of cells is named IL-17+Foxp3+Treg cells, which is an intermediate cells group between Th17 and Treg cells. The mechanisms of IL-17 promoting the growth of DLBCL cells are as follows: (1) IL-17 promotes the formation of tumor angiogenesis. (2) IL-17 promotes the expression of tumor apoptotic suppressor p53. These two mechanisms are confirmed. (3) IL-17 may trigger the pathway of TPL2/MAPK by binding to IL-17R. DLBCL, diffuse large B-cell lymphoma; Foxp3, forkhead box P3; IL-17, interleukin-17; IL-6, interleukin-6; MAPK, mitogen-activated protein kinase; Th17, T helper 17; TPL2, tumor progression locus 2; Treg, regulatory T.