mango
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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 A Leadbetter & Mikael C I Karlsson
Nature Immunology (2016) doi:10.1038/ni.3583
Published online 31 October 2016
Abstract
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.
Subject terms: Autoimmunity, Inflammation, Innate immune cells
http://www.nature.com/ni/journal/vaop/ncurrent/full/ni.3583.html
Thomas Hägglöf, Saikiran K Sedimbi, Jennifer L Yates, Roham Parsa, Briana Hauff Salas, Robert A Harris, Elizabeth A Leadbetter & Mikael C I Karlsson
Nature Immunology (2016) doi:10.1038/ni.3583
Published online 31 October 2016
Abstract
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.
Subject terms: Autoimmunity, Inflammation, Innate immune cells
http://www.nature.com/ni/journal/vaop/ncurrent/full/ni.3583.html