{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T21:30:48Z","timestamp":1792099848465,"version":"4.4.0"},"reference-count":91,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2014,12,1]],"date-time":"2014-12-01T00:00:00Z","timestamp":1417392000000},"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":[[2014,12,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Class-switch DNA recombination (CSR) and somatic hypermutation (SHM), which require activation-induced cytidine deaminase (AID), and plasma cell differentiation, which requires B lymphocyte\u2013induced maturation protein-1 (Blimp-1), are critical for the generation of class-switched and hypermutated (mature) Ab and autoantibody responses. We show that histone deacetylase inhibitors valproic acid and butyrate dampened AICDA\/Aicda (AID) and PRDM1\/Prdm1 (Blimp-1) mRNAs by upregulating miR-155, miR-181b, and miR-361 to silence AICDA\/Aicda, and miR-23b, miR-30a, and miR-125b to silence PRDM1\/Prdm1, in human and mouse B cells. This led to downregulation of AID, Blimp-1, and X-box binding protein 1, thereby inhibiting CSR, SHM, and plasma cell differentiation without altering B cell viability or proliferation. The selectivity of histone deacetylase inhibitor\u2013mediated silencing of AICDA\/Aicda and PRDM1\/Prdm1 was emphasized by unchanged expression of HoxC4 and Irf4 (important inducers\/modulators of AICDA\/Aicda), Rev1 and Ung (central elements for CSR\/SHM), and Bcl6, Bach2, or Pax5 (repressors of PRDM1\/Prdm1 expression), as well as unchanged expression of miR-19a\/b, miR-20a, and miR-25, which are not known to regulate AICDA\/Aicda or PRDM1\/Prdm1. Through these B cell\u2013intrinsic epigenetic mechanisms, valproic acid blunted class-switched and hypermutated T-dependent and T-independent Ab responses in C57BL\/6 mice. In addition, it decreased class-switched and hypermutated autoantibodies, ameliorated disease, and extended survival in lupus MRL\/Faslpr\/lpr mice. Our findings outline epigenetic mechanisms that modulate expression of an enzyme (AID) and transcription factors (Blimp-1 and X-box binding protein 1) that are critical to the B cell differentiation processes that underpin Ab and autoantibody responses. They also provide therapeutic proof-of-principle in autoantibody-mediated autoimmunity.<\/jats:p>","DOI":"10.4049\/jimmunol.1401702","type":"journal-article","created":{"date-parts":[[2014,11,13]],"date-time":"2014-11-13T04:24:01Z","timestamp":1415852641000},"page":"5933-5950","source":"Crossref","is-referenced-by-count":123,"title":["Histone Deacetylase Inhibitors Upregulate B Cell microRNAs That Silence AID and Blimp-1 Expression for Epigenetic Modulation of Antibody and Autoantibody Responses"],"prefix":"10.1093","volume":"193","author":[{"given":"Clayton A","family":"White","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas School of Medicine, University of Texas Health Science Center at San Antonio , San Antonio, TX 78229"},{"name":"Institute for Immunology, University of California , Irvine, CA 92697"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Egest J","family":"Pone","sequence":"additional","affiliation":[{"name":"Institute for Immunology, University of California , Irvine, CA 92697"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tonika","family":"Lam","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas School of Medicine, University of Texas Health Science Center at San Antonio , San Antonio, TX 78229"},{"name":"Institute for Immunology, University of California , Irvine, CA 92697"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Connie","family":"Tat","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas School of Medicine, University of Texas Health Science Center at San Antonio , San Antonio, TX 78229"},{"name":"Institute for Immunology, University of California , Irvine, CA 92697"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ken L","family":"Hayama","sequence":"additional","affiliation":[{"name":"Institute for Immunology, University of California , Irvine, CA 92697"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guideng","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas School of Medicine, University of Texas Health Science Center at San Antonio , San Antonio, TX 78229"},{"name":"Institute for Immunology, University of California , Irvine, CA 92697"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong","family":"Zan","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas School of Medicine, University of Texas Health Science Center at San Antonio , San Antonio, TX 78229"},{"name":"Institute for Immunology, University of California , Irvine, CA 92697"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paolo","family":"Casali","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Texas School of Medicine, University of Texas Health Science Center at San Antonio , San Antonio, TX 78229"},{"name":"Institute for Immunology, University of California , Irvine, CA 92697"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2014,12,15]]},"reference":[{"key":"2025030707502473500_r1","doi-asserted-by":"crossref","first-page":"517","DOI":"10.1038\/nri3216","article-title":"Immunoglobulin class-switch DNA recombination: induction, targeting and beyond","volume":"12","author":"Xu","year":"2012","journal-title":"Nat. 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