{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T21:30:34Z","timestamp":1791063034421,"version":"4.1.0"},"reference-count":72,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2000,7,1]],"date-time":"2000-07-01T00:00:00Z","timestamp":962409600000},"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":[[2000,7,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>CD153 (CD30 ligand) is a member of the TNF ligand\/cytokine family expressed on the surface of human B cells. Upon exposure to IL-4, a critical Ig class switch-inducing cytokine, Ag-activated T cells express CD30, the CD153 receptor. The observation that dysregulated IgG, IgA, and\/or IgE production is often associated with up-regulation of T cell CD30 prompted us to test the hypothesis that engagement of B cell CD153 by T cell CD30 modulates Ig class switching. In this study, we show that IgD+ IgM+ B cells up-regulate CD153 in the presence of CD154 (CD40 ligand), IL-4, and B cell Ag receptor engagement. In these cells, CD153 engagement by an agonistic anti-CD153 mAb or T cell CD30 inhibits S\u03bc\u2192S\u03b3, S\u03bc\u2192S\u03b1, and S\u03bc\u2192S\u03b5 class switch DNA recombination (CSR). This inhibition is associated with decreased TNFR-associated factor-2 binding to CD40, decreased NF-\u03baB binding to the CD40-responsive element of the C\u03b33 promoter, decreased I\u03b33-C\u03b33 germline gene transcription, and decreased expression of Ku70, Ku80, DNA protein kinase, switch-associated protein-70, and Msh2 CSR-associated transcripts. In addition, CD153 engagement inhibits IgG, IgA, and IgE production, and this effect is associated with reduced levels of B lymphocyte maturation protein-1 transcripts, and increased binding of B cell-specific activation protein to the Ig 3\u2032 enhancer. These findings suggest that CD30+ T cells modulate CSR as well as IgG, IgA, and IgE production by inducing reverse signaling through B cell CD153.<\/jats:p>","DOI":"10.4049\/jimmunol.165.2.786","type":"journal-article","created":{"date-parts":[[2014,4,22]],"date-time":"2014-04-22T03:02:33Z","timestamp":1398135753000},"page":"786-794","source":"Crossref","is-referenced-by-count":74,"title":["Engagement of CD153 (CD30 Ligand) by CD30+ T Cells Inhibits Class Switch DNA Recombination and Antibody Production in Human IgD+ IgM+ B Cells"],"prefix":"10.1093","volume":"165","author":[{"given":"Andrea","family":"Cerutti","sequence":"first","affiliation":[{"name":"Division of Molecular Immunology, Department of Pathology, Weill Medical College of Cornell University , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andra\u0300s","family":"Schaffer","sequence":"additional","affiliation":[{"name":"Division of Molecular Immunology, Department of Pathology, Weill Medical College of Cornell University , New York, NY 10021"},{"name":"The Immunology Program, Cornell University Weill Graduate School of Medical Sciences , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raymond G","family":"Goodwin","sequence":"additional","affiliation":[{"name":"Immunex Corporation , Seattle, WA 98101"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shefali","family":"Shah","sequence":"additional","affiliation":[{"name":"Division of Molecular Immunology, Department of Pathology, Weill Medical College of Cornell University , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong","family":"Zan","sequence":"additional","affiliation":[{"name":"Division of Molecular Immunology, Department of Pathology, Weill Medical College of Cornell University , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Scott","family":"Ely","sequence":"additional","affiliation":[{"name":"Division of Molecular Immunology, Department of Pathology, Weill Medical College of Cornell University , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paolo","family":"Casali","sequence":"additional","affiliation":[{"name":"Division of Molecular Immunology, Department of Pathology, Weill Medical College of Cornell University , New York, NY 10021"},{"name":"The Immunology Program, Cornell University Weill Graduate School of Medical Sciences , New York, NY 10021"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2000,7,15]]},"reference":[{"key":"2025032907480369400_R1","first-page":"2318","volume-title":"J. 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