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. 2003 Mar 29;24(4):207–212. doi: 10.1016/S1471-4906(03)00067-X

Fig. 2.

Fig. 2

Current working hypothesis for the regulation of Th1 development by IL-12 family members and by IL-18. On infection or pathogen uptake (green symbols in APC), APCs secrete cytokines, which act on Th cells at different stages of their development. IL-27 appears to activate Th0 and Th0/1 cells, which express WSX-1 (identical with TCCR). After induction of IL-12Rβ2 expression IL-12 is able to drive further differentiation and maintenance of Th1eff cells. Homodimeric p40 is able to antagonize IL-12 at its receptor or to contribute to Th1 activation by interacting with IL-12Rβ1 and possibly a putative second receptor component. IL-23 is able to activate Th1mem cells. There is synergy between IL-27 and IL-12, as well as between IL-12 and IL-18. IL-12 induces the receptor for IL-18 on Th cells [66]. The receptors for IL-12 and IL-23 are also expressed on APCs or APC subpopulations (not shown in this figure). Thus, regulation of APC activity might be modulated, as well as T-cell development, by IL-12 and IL-23. Abbreviations: APC, antigen-presenting cell; IL-12, interleukin-12; R, receptor; Th0, naı̈ve T cells; Th0/1, differentiating naı̈ve T cells; Th1eff, effector T; Th1mem, memory Th1.