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Cytokines

GM-CSF in focus

Nature Reviews Immunology volume 11, pages 370–371 (2011)Cite this article

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Studies by Codarri et al. revealed that IL-23 induces GM-CSF secretion by helper T cells and that neutralization of IL-12 and IFNγ results in increased GM-CSF expression in activated T cells. Strikingly, activated autoreactive CD4+T cells that secreted GM-CSF initiated more severe experimental autoimmune encephalomyelitis (EAE) than IFNγ- or IL-17-secreting T cells. Moreover, both TH1 and TH17 cells were shown to rely on GM-CSF secretion for their pathogenicity in GM-CSF neutralization studies. These findings suggest that GM-CSF mediates the encephalitogenic function of both effector TH1 and TH17 cells.

Strikingly, treatment of mice with GM-CSF-neutralizing antibody after the onset of EAE abolished the disease symptoms and prevented relapses. Moreover, T cells from GM-CSF-deficient mice migrated to the CNS but, in contrast to wild-type T cells, failed to accumulate. Further analysis showed that T cell-derived GM-CSF contributes to CNS inflammation by recruiting myeloid antigen-presenting cells (APCs). Finally, GM-CSF-secreting CD4+ T cells were shown to express retinoic acid receptor-related orphan receptor-γt (RORγt), and RORγt-deficient T cells failed to produce GM-CSF, whereas induction of RORγt expression resulted in GM-CSF expression. So, Codarri et al. suggest that RORγt is involved in the regulation of GM-CSF.

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ORIGINAL RESEARCH PAPERS

  1. Codarri, L. et al. RORγt drives production of the cytokine GM-CSF in helper T cells, which is essential for the effector phase of autoimmune neuroinflammation. Nature Immunol. 123, 123–456 (2011)

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  2. El-Behi, M. et al. The encephalitogenicity of TH17 cells is dependent on IL-1- and IL-23-induced production of the cytokine GM-CSF. Nature Immunol. 123, 123–456 (2011)

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Authors
  1. Maria Papatriantafyllou
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Papatriantafyllou, M. GM-CSF in focus. Nat Rev Immunol 11, 370–371 (2011). https://doi.org/10.1038/nri2996

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