Journal
NATURE IMMUNOLOGY
Volume 17, Issue 12, Pages 1407-1414Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.3583
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Funding
- Swedish Research Council
- Center for Allergy Research Karolinska Institutet
- Swedish Medical Society
- King Gustaf V's 80-year Foundation
- Magnus Bergvall Foundation
- Karolinska Institutet
- Erik and Edith Fernstrom foundation
- Swedish Society for Medical Research
- Centre for Allergy Research
- Ellen, Walter and Lennart Hesselman foundation
- O.E. and Edla Johansson's Foundation
- Tore Nilsson's foundation
- Karolinska Institutet's foundations
- US National Institutes of Health [AI104788-01A1]
- Trudeau Institute
- University of Texas Health Science Center at San Antonio
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The innate responsiveness of the immune system is important not only for quick responses to pathogens but also for the initiation and shaping of the subsequent adaptive immune response. Activation via the cytokine IL-18, a product of inflammasomes, gives rise to a rapid response that includes the production of self-reactive antibodies. As increased concentrations of this cytokine are found in inflammatory diseases, we investigated the origin of the B cell response and its regulation. We identified an accumulation of B cell helper neutrophils in the spleen that interacted with innate-type invariant natural killer T cells (iNKT cells) to regulate B cell responses. We found that neutrophil-dependent expression of the death-receptor ligand FasL by iNKT cells was needed to restrict autoantibody production. Neutrophils can thus license MKT cells to regulate potentially harmful autoreactive B cell responses during inflammasome-driven inflammation.
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