{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,19]],"date-time":"2026-05-19T09:39:35Z","timestamp":1779183575799,"version":"3.51.4"},"reference-count":39,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[1999,3,1]],"date-time":"1999-03-01T00:00:00Z","timestamp":920246400000},"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":[[1999,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Murine models of allergen-induced pulmonary inflammation share many features with human asthma, including the development of antigen-induced pulmonary eosinophilia, airway hyperresponsiveness, antigen-specific cellular and antibody responses, the elaboration of Th2 cytokines (interleukin [IL]-4 and IL-5), and the expression of chemokines with activity for eosinophils. We examined the role of B cells and antigen-specific antibody responses in such a model by studying the histopathologic and physiologic responses of B cell\u2013deficient mice compared with wild-type controls, following systemic immunization and airway challenge with ovalbumin (OVA). Both OVA-challenged wild-type and B cell\u2013deficient mice developed (1) airway hyperresponsiveness, (2) pulmonary inflammation with activated T cells and eosinophils, (3) IL-4 and IL-5 secretion into the airway lumen, and (4) increased expression of the eosinophil active chemokines eotaxin and monocyte chemotactic protein-3. There were no significant differences in either the pathologic or physiologic responses in the B cell\u2013deficient mice compared with wild-type mice. These data indicate that B cells and antigen-specific antibodies are not required for the development of airway hyperresponsiveness, eosinophilic pulmonary inflammation, and chemokine expression in sensitized mice following aerosol challenge with antigen.<\/jats:p>","DOI":"10.1165\/ajrcmb.20.3.3291","type":"journal-article","created":{"date-parts":[[2013,4,3]],"date-time":"2013-04-03T21:53:09Z","timestamp":1365025989000},"page":"379-387","source":"Crossref","is-referenced-by-count":72,"title":["Antigen-Induced Airway Hyperresponsiveness, Pulmonary Eosinophilia, and Chemokine Expression in B Cell\u2013Deficient Mice"],"prefix":"10.1093","volume":"20","author":[{"given":"James A.","family":"MacLean","sequence":"first","affiliation":[{"name":"Clinical Immunology and Allergy Unit and Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital; Partners Asthma Center; and Harvard Medical School, Boston, Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Alain","family":"Sauty","sequence":"additional","affiliation":[{"name":"Clinical Immunology and Allergy Unit and Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital; Partners Asthma Center; and Harvard Medical School, Boston, Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Andrew D.","family":"Luster","sequence":"additional","affiliation":[{"name":"Clinical Immunology and Allergy Unit and Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital; Partners Asthma Center; and Harvard Medical School, Boston, Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jeffrey M.","family":"Drazen","sequence":"additional","affiliation":[{"name":"Clinical Immunology and Allergy Unit and Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital; Partners Asthma Center; and Harvard Medical School, Boston, Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"George T.","family":"De Sanctis","sequence":"additional","affiliation":[{"name":"Clinical Immunology and Allergy Unit and Infectious Disease Unit, Department of Medicine, Massachusetts General Hospital; Pulmonary and Critical Care Divisions, Department of Medicine, Brigham and Women's Hospital; Partners Asthma Center; and Harvard Medical School, Boston, Massachusetts"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[1999,3,1]]},"reference":[{"key":"2026030700134991200_B1","doi-asserted-by":"crossref","first-page":"374","DOI":"10.1164\/ajrccm\/146.2.374","article-title":"CD4+ T-lymphocytes and interleukin-5 mediate antigen-induced eosinophil infiltration into the mouse trachea.","volume":"146","author":"Nakajima","year":"1992","journal-title":"Am. 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