Frontiers in immunology · 2020
SIRPα on Mouse B1 Cells Restricts Lymphoid Tissue Migration and Natural Antibody Production.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Franke Katka, Pillai Saravanan Y, Hoogenboezem Mark, Gijbels Marion J J, Matlung Hanke L, Geissler Judy, Olsman Hugo, Pottgens Chantal, van Gorp Patrick J, Ozsvar-Kozma Maria, Saito Yasuyuki, Matozaki Takashi, Kuijpers Taco W, Hendriks Rudi W, Kraal Georg, Binder Christoph J, de Winther Menno P J, van den Berg Timo K
Аннотация
The inhibitory immunoreceptor SIRPα is expressed on myeloid and neuronal cells and interacts with the broadly expressed CD47. CD47-SIRPα interactions form an innate immune checkpoint and its targeting has shown promising results in cancer patients. Here, we report expression of SIRPα on B1 lymphocytes, a subpopulation of murine B cells responsible for the production of natural antibodies. Mice defective in SIRPα signaling (SIRPαΔCYT mice) displayed an enhanced CD11b/CD18 integrin-dependent B1 cell migration from the peritoneal cavity to the spleen, local B1 cell accumulation, and enhanced circulating natural antibody levels, which was further amplified upon immunization with T-independent type 2 antigen. As natural antibodies are atheroprotective, we investigated the involvement of SIRPα signaling in atherosclerosis development. Bone marrow (SIRPαΔCYT>LDLR-/-) chimaeric mice developed reduced atherosclerosis accompanied by increased natural antibody production. Collectively, our data identify SIRPα as a unique B1 cell inhibitory receptor acting to control B1 cell migration, and imply SIRPα as a potential therapeutic target in atherosclerosis.