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dc.contributor.authorOrdoñez, Ciara
dc.contributor.authorSavage, Hannah P
dc.contributor.authorTarajia, Musharaf
dc.contributor.authorRivera, René
dc.contributor.authorWeeks‐Galindo, Cheyenne
dc.contributor.authorSambrano, Dilcia
dc.contributor.authorRiley, Lee
dc.contributor.authorFernandez, Patricia L
dc.contributor.authorBaumgarth, Nicole
dc.contributor.authorGoodridge, Amador
dc.date.accessioned2020-08-05T22:50:32Z
dc.date.available2020-08-05T22:50:32Z
dc.date.issued2018-02-08
dc.identifier.otherdoi:10.1111/imm.12909
dc.identifier.urihttp://repositorio-indicasat.org.pa/handle/123456789/225
dc.descriptionTuberculosis is an infectious disease caused by Mycobacterium tuberculosis. The cellular immune response to mycobacteria has been characterized extensively, but the antibody response remains underexplored. The present study aimed to examine whether host or bacterial phospholipids induce secretion of IgM, and specifically anti-phospholipid IgM, antibodies by B cells and to identify the responsible B-cell subset. Here we show that peritoneal B cells responded to lipid antigens by secreting IgM antibodies. Specifically, stimulation with M. tuberculosis H37Rv total lipids resulted in significant induction of total and anti-phosphatidylcholine IgM. Similarly, IgM antibody production increased significantly with stimulation by whole Mycobacterium bovis bacillus Calmette–Guerin. The B-1 subset was the dominant source of IgM antibodies after exposure to cardiolipin. Both CD5+ B-1a and CD5 B-1b cell subsets secreted total IgM antibodies after exposure to M. tuberculosis H37Rv total lipids in vitro. Overall, our results suggest that the poly-reactive B-1 cell repertoire contributes to non-specific anti-phospholipid IgM antibody secretion in response to M. tuberculosis lipids.en_US
dc.description.abstractTuberculosis is an infectious disease caused by Mycobacterium tuberculosis. The cellular immune response to mycobacteria has been characterized extensively, but the antibody response remains underexplored. The present study aimed to examine whether host or bacterial phospholipids induce secretion of IgM, and specifically anti-phospholipid IgM, antibodies by B cells and to identify the responsible B-cell subset. Here we show that peritoneal B cells responded to lipid antigens by secreting IgM antibodies. Specifically, stimulation with M. tuberculosis H37Rv total lipids resulted in significant induction of total and anti-phosphatidylcholine IgM. Similarly, IgM antibody production increased significantly with stimulation by whole Mycobacterium bovis bacillus Calmette–Guerin. The B-1 subset was the dominant source of IgM antibodies after exposure to cardiolipin. Both CD5+ B-1a and CD5 B-1b cell subsets secreted total IgM antibodies after exposure to M. tuberculosis H37Rv total lipids in vitro. Overall, our results suggest that the poly-reactive B-1 cell repertoire contributes to non-specific anti-phospholipid IgM antibody secretion in response to M. tuberculosis lipids.en_US
dc.language.isoengen_US
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectactivationen_US
dc.subjectautoantibodiesen_US
dc.subjectB cellsen_US
dc.subjectbacterialen_US
dc.subjectinnate lymphoid cellsen_US
dc.titleBoth B-1a and B-1b cells exposed to Mycobacterium tuberculosis lipids differentiate into IgM antibody-secreting cellsen_US
dc.typeinfo:eu-repo/semantics/articleen_US
dc.typeinfo:edu-repo/semantics/publishedVersion


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