{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,21]],"date-time":"2026-05-21T18:13:06Z","timestamp":1779387186289,"version":"3.53.1"},"reference-count":49,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2019,1,1]],"date-time":"2019-01-01T00:00:00Z","timestamp":1546300800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,1,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Engagement of the BCR with Ags triggers signaling pathways for commitment of B lymphocyte responses that can be regulated, in part, by reactive oxygen species. To investigate the functional relevance of reactive oxygen species produced in primary B cells, we focused on the role of the hydrogen peroxide generator Duox1 in stimulated splenic B cells under the influence of the TH2 cytokine IL-4. We found that H2O2 production in wild type (WT) and Nox2-deficient CD19+ B cells was boosted concomitantly with enhanced expression of Duox1 following costimulation with BCR agonists together with IL-4, whereas stimulated Duox1\u2212\/\u2212 cells showed attenuated H2O2 release. We examined whether Duox1-derived H2O2 contributes to proliferative activity and Ig isotype production in CD19+ cells upon BCR stimulation. Duox1\u2212\/\u2212 CD19+ B cells showed normal responses of Ig production but a higher rate of proliferation than WT or Nox2-deficient cells. Furthermore, we demonstrated that the H2O2 scavenger catalase mimics the effect of Duox1 deficiency by enhancing proliferation of WT CD19+ B cells in vitro. Results from immunized mice reflected the in vitro observations: T cell\u2013independent Ag induced increased B cell expansion in germinal centers from Duox1\u2212\/\u2212 mice relative to WT and Nox2\u2212\/\u2212 mice, whereas immunization with T cell\u2013dependent or \u2013independent Ag elicited normal Ig isotype secretion in the Duox1 mutant mice. These observations, obtained both by in vitro and in vivo approaches, strongly suggest that Duox1-derived hydrogen peroxide negatively regulates proliferative activity but not Ig isotype production in primary splenic CD19+ B cells.<\/jats:p>","DOI":"10.4049\/jimmunol.1601395","type":"journal-article","created":{"date-parts":[[2018,12,17]],"date-time":"2018-12-17T22:35:27Z","timestamp":1545086127000},"page":"428-440","source":"Crossref","is-referenced-by-count":10,"title":["Duox1 Regulates Primary B Cell Function under the Influence of IL-4 through BCR-Mediated Generation of Hydrogen Peroxide"],"prefix":"10.1093","volume":"202","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7204-4702","authenticated-orcid":false,"given":"Ryuichi","family":"Sugamata","sequence":"first","affiliation":[{"name":"Molecular Defense Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Rockville, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Agnes","family":"Donko","sequence":"additional","affiliation":[{"name":"Molecular Defense Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Rockville, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yousuke","family":"Murakami","sequence":"additional","affiliation":[{"name":"Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Rockville, MD 20852"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Howard E","family":"Boudreau","sequence":"additional","affiliation":[{"name":"Molecular Defense Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Rockville, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chen-Feng","family":"Qi","sequence":"additional","affiliation":[{"name":"Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Rockville, MD 20852"},{"name":"Pathology Core, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Rockville, MD 20852"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2452-4111","authenticated-orcid":false,"given":"Jaeyul","family":"Kwon","sequence":"additional","affiliation":[{"name":"Molecular Defense Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Rockville, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5463-1583","authenticated-orcid":false,"given":"Thomas L","family":"Leto","sequence":"additional","affiliation":[{"name":"Molecular Defense Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Rockville, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2019,1,15]]},"reference":[{"key":"2025030417560139800_r1","doi-asserted-by":"crossref","first-page":"21","DOI":"10.1146\/annurev.immunol.021908.132541","article-title":"B cell signaling and fate decision","volume":"28","author":"Kurosaki","year":"2010","journal-title":"Annu. 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