RORγt drives production of the cytokine GM-CSF in helper T cells, which is essential for the effector phase of autoimmune neuroinflammation

By L. Codarri, Gabor Gyülveszi, V. Tosevski, Lysann Hesske, A. Fontana, L. Magnenat, T. Suter, B. Becher. Nature Immunology, 2011

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Subfields: Immunology

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Innate immunity in the central nervous system. (2012, positive): “GM-CSF GM-CSF is required to recruit CD11b + myeloid cells, which are thought to sustain local CNS inflammation, mediate direct myelin damage, and support the survival of lymphocytes (112–114).”
Th17 cells: biology, pathogenesis of autoimmune and inflammatory diseases, and therapeutic strategies. (2012, background): “The GM-CSF in turn acts on APC (and in particular by CD103+ dermal DCs) to stimulate the secretion of IL-23 and activation of encephalitogenic T cells, setting a positive feedback loop during inflammation.82-84 In consensus, absence of GM-CSF conferred resistance to EAE in mice, even in the presence”
Microbiota-Dependent Crosstalk Between Macrophages and ILC3 Promotes Intestinal Homeostasis (2014, positive): “RORγt+ T helper 17 (TH17) cells can produce large amounts of Csf2 in the inflamed brain and intestine (26, 27, 32).”
Efficient clearance of early apoptotic cells by human macrophages requires “M2c” polarization and MerTK induction (2012, background): “From this perspective, production of M-CSF by Tregs might counterbalance the well-known production of GM-CSF by proinflammatory Th1 and Th17 lymphocytes (51), with strong and direct repercussions of the Treg versus Th17 balance on M-CSF versus GM-CSF macrophage differentiation.”