Hirota, K. et al. Plasticity of Th17 cells in Peyer’s patches is responsible for the induction of T cell-dependent IgA responses. Nat. Immunol. 14, 372-379

1] Division of Molecular Immunology, Medical Research Council National Institute for Medical Research, Mill Hill, London, UK. [2].
Nature Immunology (Impact Factor: 20). 03/2013; 14(4). DOI: 10.1038/ni.2552
Source: PubMed


Intestinal Peyer's patches are essential lymphoid organs for the generation of T cell-dependent immunoglobulin A (IgA) for gut homeostasis. Through the use of interleukin 17 (IL-17) fate-reporter mice, we found here that endogenous cells of the TH17 subset of helper T cells in lymphoid organs of naive mice 'preferentially' homed to the intestines and were maintained independently of IL-23. In Peyer's patches, such TH17 cells acquired a follicular helper T cell (TFH cell) phenotype and induced the development of IgA-producing germinal center B cells. Mice deficient in TH17 cells failed to generate antigen-specific IgA responses, which provides evidence that TH17 cells are the crucial subset required for the production of high-affinity T cell-dependent IgA.

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    • "Recent studies have highlighted novel roles for effector T cell subsets, such as Th17 and Tfh cells, in ectopic lymphoid neogenesis and the control of GC reactions (Lu et al., 2011; Peters et al., 2011; Rangel-Moreno et al., 2011; Hirota et al., 2013). Thus, cytokines linked with either T cell differentiation or plasticity of effector T cells into Tfh-like phenotypes may regulate ELS involvement in chronic disease (Lu et al., 2011; Peters et al., 2011; Hirota et al., 2013). As IL-27 inhibits effector Th17 responses, we considered the expression of Th17 and Tfh cell markers within the inflamed synovium. "
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    • "This suggestion is somewhat controversial, as recent studies have implicated Th17 cells rather than Tregs in the induction of IgA in the gut (22, 23). Cao et al. implicated the mammalian specific cytokine IL17a in the production of IgA to flagellin. "
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    • "Nossent, Australia). IL-17 is a known proinflammatory cytokine produced by T cells in order to recruit monocytes and neutrophils to the site of inflammation [28] [29] along with other Th17 cytokines [29] [30] [31] [32] [33] [34], and it is currently under investigation in several clinical studies as target of anti-inflammatory therapies for diseases such as psoriasis and multiple sclerosis [35]. Another cellular mechanism studied for its possible involvement in SLE is the identification of abnormalities of plasmacytoid dendritic cells that contribute to disease onset (V. "
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