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Mice deficient in B1 cells (<jats:italic>xid<\/jats:italic>), or activation\u2010induced cytidine deaminase (<jats:italic><jats:styled-content style=\"fixed-case\">AID<\/jats:styled-content><\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>), or invariant natural killer T (<jats:styled-content style=\"fixed-case\">iNKT<\/jats:styled-content>) cells (<jats:italic>J\u03b118<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>), or interleukin\u201013 (<jats:italic><jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201013<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup>) had impaired early clearance of pneumococci in the lung, compared with wild\u2010type mice. In contrast, <jats:italic><jats:styled-content style=\"fixed-case\">AID<\/jats:styled-content><\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice adoptively transferred with <jats:italic><jats:styled-content style=\"fixed-case\">AID<\/jats:styled-content><\/jats:italic><jats:sup>+\/+<\/jats:sup> B1a cells, significantly cleared bacteria from the lungs as early as 3\u00a0days post infection. We show that this early bacterial clearance corresponds to an allergic contact sensitivity\u2010like cutaneous response, probably due to a subpopulation of initiating B1a cells. In the pneumonia model, these B1a cells were found to secrete higher affinity antigen\u2010specific IgM. In addition, as in contact sensitivity, <jats:styled-content style=\"fixed-case\">iNKT<\/jats:styled-content> cells were required for the anti\u2010pneumococcal B1a cell initiating response, probably through early production of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201013, given that <jats:italic><jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201013<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> mice also failed to clear infection. Our study is the first to demonstrate the importance of <jats:styled-content style=\"fixed-case\">AID<\/jats:styled-content> in generating an appropriate B1a cell response to pathogenic bacteria. Given the antibody affinity and pneumonia resistance data, natural IgM produced by conventional B1a cells are not responsible for pneumonia clearance compared with the <jats:styled-content style=\"fixed-case\">AID<\/jats:styled-content>\u2010dependent subset.<\/jats:p>","DOI":"10.1111\/imm.12544","type":"journal-article","created":{"date-parts":[[2015,10,12]],"date-time":"2015-10-12T22:42:03Z","timestamp":1444689723000},"page":"97-113","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":24,"title":["Expression of activation\u2010induced cytidine deaminase enhances the clearance of pneumococcal pneumonia: evidence of a subpopulation of protective anti\u2010pneumococcal B1a cells"],"prefix":"10.1111","volume":"147","author":[{"given":"Natsuo","family":"Yamamoto","sequence":"first","affiliation":[{"name":"Section\u00a0of Allergy and Clinical Immunology Department of Internal Medicine Yale University School of Medicine New Haven CT 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