Neutrophils license iNKT cells to regulate self-reactive mouse B cell responses

Thomas Hägglöf, Saikiran K. Sedimbi, Jennifer L. Yates, Roham Parsa, Briana Hauff Salas, Robert A. Harris, Elizabeth Leadbetter, Mikael C.I. Karlsson

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


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 iNKT cells to regulate potentially harmful autoreactive B cell responses during inflammasome-driven inflammation.

Original languageEnglish (US)
Pages (from-to)1407-1414
Number of pages8
JournalNature Immunology
Issue number12
StatePublished - Dec 1 2016

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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