Experimental priming of encephalitogenic Th1/Th17 cells requires pertussis toxin-driven IL-1β production by myeloid cells

Francesca Ronchi, Camilla Basso, Silvia Preite, Andrea Reboldi, Dirk Baumjohann, Luana Perlini, Antonio Lanzavecchia and Federica Sallusto ()
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Francesca Ronchi: Cellular Immunology Laboratory and Immune Regulation Laboratory, Institute for Research in Biomedicine, Università della Svizzera italiana
Camilla Basso: Cellular Immunology Laboratory and Immune Regulation Laboratory, Institute for Research in Biomedicine, Università della Svizzera italiana
Silvia Preite: Cellular Immunology Laboratory and Immune Regulation Laboratory, Institute for Research in Biomedicine, Università della Svizzera italiana
Andrea Reboldi: Cellular Immunology Laboratory and Immune Regulation Laboratory, Institute for Research in Biomedicine, Università della Svizzera italiana
Dirk Baumjohann: Cellular Immunology Laboratory and Immune Regulation Laboratory, Institute for Research in Biomedicine, Università della Svizzera italiana
Luana Perlini: Cellular Immunology Laboratory and Immune Regulation Laboratory, Institute for Research in Biomedicine, Università della Svizzera italiana
Antonio Lanzavecchia: Cellular Immunology Laboratory and Immune Regulation Laboratory, Institute for Research in Biomedicine, Università della Svizzera italiana
Federica Sallusto: Cellular Immunology Laboratory and Immune Regulation Laboratory, Institute for Research in Biomedicine, Università della Svizzera italiana

Nature Communications, 2016, vol. 7, issue 1, 1-11

Abstract: Abstract CD4+ Th17 are heterogeneous in terms of cytokine production and capacity to initiate autoimmune diseases, such as experimental autoimmune encephalomyelitis (EAE). Here we demonstrate that experimental priming of encephalitogenic Th cells expressing RORγt and T-bet and producing IL-17A, IFN-γ and GM-CSF but not IL-10 (Th1/Th17), is dependent on the presence of pertussis toxin (PTX) at the time of immunization. PTX induces early production of IL-1β by CD11b+CCR2+Gr1+ myeloid cells, which are rapidly recruited to antigen-draining lymph nodes. PTX-induced generation of Th1/Th17 cells is impaired in IL-1β- and ASC-deficient mice and in mice in which myeloid cells are depleted or fail to migrate to lymph nodes and requires expression of IL-1R1 and MyD88 on both T cells and non-T cells. Collectively, these data shed light on the enigmatic function of PTX in EAE induction and suggest that inflammatory monocytes and microbial infection can influence differentiation of pathogenic Th1/Th17 cells in autoimmune diseases through production of IL-1β.

Date: 2016
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DOI: 10.1038/ncomms11541

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