Skip to main content
. Author manuscript; available in PMC: 2010 Aug 3.
Published in final edited form as: Ann N Y Acad Sci. 2010 Jan;1183:211–221. doi: 10.1111/j.1749-6632.2009.05133.x

Figure 2.

Figure 2

Sequential recruitment of effector T cells into the target organ during inflammation (reprinted with permission from Dardalhon et al.79). In secondary lymphoid tissues, IL-6 together with transforming growth factor (TGF)-β can induce IL-21 production from IL-17-producing T cells. IL-21 then functions in an autocrine self-amplification loop to increase the T helper (Th)17 response. The maintenance of already committed Th17 cells requires IL-23. Th17 cells would then constitute the first wave of effector T cells migrating to the target tissue. IL-17 secretion will induce the expression of different chemokines, which could drive the migration of further waves of effector T cells and also mononuclear cells. Finally, this change in the composition of the effector T cells toward Th1 contributes to resolution of tissue inflammation by regulatory T cells (Tregs). IFN-γ, interferon-γ.