BACKGROUND Interleukin-4 (IL-4) is widely recognized as the canonical marker for Th2-polarized CD4+ T cells.1 IL-4 was originally identified by its function as a B cell–stimulating factor, and numerous in vivo models of infection concur that IL-4 is critical for the isotype switch of B cells to IgE and IgG1. IL-4 also promotes the Th2 polarization of naive CD4+ T cells in vitro. However, in vivo studies have found that Th2 cells can develop in mice deficient for IL-4, the IL-4Ralpha chain, or the IL-4R–associated Stat 6. Stat6 has been shown to play a central role in mediating the immune regulatory signal of IL-4.2 Collectively, these observations suggest that IL-4 production in sentinel lymph nodes draining a site of infection may be more important to support type 2 B cell responses rather than to establish the underlying Th2 response. Therefore, it stands to reason that the production of IL-4 by Th2 cells should preferentially occur in B cell follicles to optimize B cell help. In addition, IL-4 can prime macrophages to undergo additional, microbial-induced changes in cellular properties, relevant to host defense and pathogenesis of infectious and immune diseases.3 IL-4 also regulates the expression of the low affinity Fc receptor for IgE (CD23) on both lymphocytes and monocytes.
1. Abbas, A.K. et al: Nature 383:787–793, 1996
2. van Panhuys, N. et al: Proc. Natl. Acad. Sci. USA. 105:12423–8, 2008
3. Varin, A. et al: Blood 115:353-62, 2010
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