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Allergen stimulation of IgE-bound Fc\u03b5RI on mast cells or basophils induces the production of chemical mediators and cytokines. In addition, IgE binding to Fc\u03b5RI without allergen promotes the survival or proliferation of these and other cells. Thus, spontaneously produced natural IgE can increase an individual\u2019s susceptibility to allergic diseases. Mice deficient in MyD88, a major TLR signaling molecule, have high serum levels of natural IgE, the mechanism for which remains unknown. In this study, we demonstrated that the high serum IgE levels were maintained from weaning by memory B cells (MBCs). IgE from plasma cells and sera from most Myd88\u2212\/\u2212 mice, but none of the Myd88+\/\u2212 mice, recognized Streptococcus azizii, a commensal bacterium overrepresented in the lungs of Myd88\u2212\/\u2212 mice. IgG1+ MBCs from the spleen also recognized S. azizii. The serum IgE levels declined with the administration of antibiotics and were boosted by challenge with S. azizii in Myd88\u2212\/\u2212 mice, indicating the contribution of S. azizii\u2013specific IgG1+ MBCs to the natural IgE production. Th2 cells were selectively increased in the lungs of Myd88\u2212\/\u2212 mice and were activated upon addition of S. azizii in the lung cells ex vivo. Finally, lung nonhematopoietic cells, and CSF1 overproduced therefrom, were responsible for natural IgE production in Myd88\u2212\/\u2212 mice. Thus, some commensal bacteria may prime the Th2 response and natural IgE production in the MyD88-defective lung environment in general.<\/jats:p>","DOI":"10.4049\/jimmunol.2200888","type":"journal-article","created":{"date-parts":[[2023,3,8]],"date-time":"2023-03-08T14:10:59Z","timestamp":1678284659000},"page":"959-972","source":"Crossref","is-referenced-by-count":6,"title":["Commensal Bacteria and the Lung Environment Are Responsible for Th2-Mediated Memory Yielding Natural IgE in MyD88-Deficient Mice"],"prefix":"10.1093","volume":"210","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5807-8722","authenticated-orcid":false,"given":"Shunsuke","family":"Amano","sequence":"first","affiliation":[{"name":"Division of Cancer Cell Biology, Research Institute for Biomedical Sciences, Tokyo University of Science , Noda, Chiba,","place":["Japan"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kei","family":"Haniuda","sequence":"additional","affiliation":[{"name":"Division of Cancer Cell Biology, Research Institute for Biomedical Sciences, Tokyo University of Science , Noda, Chiba,","place":["Japan"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Saori","family":"Fukao","sequence":"additional","affiliation":[{"name":"Division of Cancer Cell Biology, Research Institute for Biomedical Sciences, Tokyo University of Science , Noda, Chiba,","place":["Japan"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7068-715X","authenticated-orcid":false,"given":"Hiroyasu","family":"Aoki","sequence":"additional","affiliation":[{"name":"Division of Molecular Regulation of Inflammatory and Immune Diseases, Research Institute for Biomedical Sciences, Tokyo University of Science , Noda, Chiba,","place":["Japan"]},{"name":"Department of Preventive Medicine, Graduate School of Medicine, The University of Tokyo , Bunkyo-ku, Tokyo,","place":["Japan"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Satoshi","family":"Ueha","sequence":"additional","affiliation":[{"name":"Division of Molecular Regulation of Inflammatory and Immune Diseases, Research Institute for Biomedical Sciences, Tokyo University of Science , Noda, Chiba,","place":["Japan"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5195-0474","authenticated-orcid":false,"given":"Daisuke","family":"Kitamura","sequence":"additional","affiliation":[{"name":"Division of Cancer Cell Biology, Research Institute for Biomedical Sciences, Tokyo University of Science , Noda, Chiba,","place":["Japan"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2023,2,20]]},"reference":[{"key":"2025021008021002800_r1","doi-asserted-by":"crossref","first-page":"1109","DOI":"10.1038\/ni.3508","article-title":"Autonomous membrane IgE signaling prevents IgE-memory formation","volume":"17","author":"Haniuda","year":"2016","journal-title":"Nat. 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