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. 2015 Jun 22;146(1):1–10. doi: 10.1111/imm.12485

Figure 2.

Figure 2

Proposed model for the capacity of α-galactosylceramide (α-GalCer) and related invariant natural killer T (iNKT) cell antigens to protect mice against experimental autoimmune encephalomyelitis. α-GalCer-activated iNKT cells produce a variety of cytokines that can promote T helper type 2 (Th2) deviation of autoreactive T-cell responses, Foxp3+ regulatory T (Treg) cells, and immunosuppressive immature [e.g. myeloid-derived suppressor cells (MDSCs)] and mature [e.g. dendritic cells (DCs), M2 macrophages] myeloid cells. Tolerogenic myeloid lineage cells may also promote the induction of Treg cells. In turn, Th2 cells, Treg cells and suppressive myeloid cells suppress the generation and/or function of pathogenic autoantigen-specific Th1, Th17 and cytotoxic T cells (CTL) in the central nervous system (CNS). GM-CSF, granulocyte–macrophage colony-stimulating factor; IFN-γ, interferon-γ; IL-4, interleukin-4; TGF-β, transforming growth factor-β.