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Gammaherpesvirus 68 infection of adult mice (an EBV model) was shown to induce polyclonal B cell activation and hypergammaglobulinemia, as well as increased production of autoantibodies. In this study, we explored the possibility that this breach of tolerance reflects loss of B cell anergy. Our findings show that, although anergic B cells transiently acquire an activated phenotype early during infection, they do not become responsive to autoantigen, as measured by the ability to mobilize Ca2+ following AgR cross-linking or mount Ab responses following immunization. Indeed, naive B cells also acquire an activated phenotype during acute infection but are unable to mount Ab responses to either T cell-dependent or T cell-independent Ags. In acutely infected animals, Ag stimulation leads to upregulation of costimulatory molecules and relocalization of Ag-specific B cells to the B\u2013T cell border; however, these cells do not proliferate or differentiate into Ab-secreting cells. Adoptive-transfer experiments show that the suppressed state is reversible and is dictated by the environment in the infected host. Finally, B cells in infected mice deficient of CD4+ T cells are not suppressed, suggesting a role for CD4+ T cells in enforcing unresponsiveness. Thus, rather than promoting loss of tolerance, gammaherpesvirus 68 infection induces an immunosuppressed state, reminiscent of compensatory anti-inflammatory response syndrome.<\/jats:p>","DOI":"10.4049\/jimmunol.1201407","type":"journal-article","created":{"date-parts":[[2012,8,18]],"date-time":"2012-08-18T05:40:11Z","timestamp":1345268411000},"page":"2965-2974","source":"Crossref","is-referenced-by-count":14,"title":["Retention of Anergy and Inhibition of Antibody Responses during Acute Gammaherpesvirus 68 Infection"],"prefix":"10.1093","volume":"189","author":[{"given":"Andrew","family":"Getahun","sequence":"first","affiliation":[{"name":"Integrated Department of Immunology, University of Colorado School of Medicine and National Jewish Health , Denver, CO 80206"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mia J","family":"Smith","sequence":"additional","affiliation":[{"name":"Integrated Department of Immunology, University of Colorado School of Medicine and National Jewish Health , Denver, CO 80206"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Igor","family":"Kogut","sequence":"additional","affiliation":[{"name":"Integrated Department of Immunology, University of Colorado School of Medicine and National Jewish Health , Denver, CO 80206"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linda F","family":"van Dyk","sequence":"additional","affiliation":[{"name":"Integrated Department of Immunology, University of Colorado School of Medicine and National Jewish Health , Denver, CO 80206"},{"name":"Department of Microbiology, University of Colorado School of Medicine , Aurora, CO 80045"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"John C","family":"Cambier","sequence":"additional","affiliation":[{"name":"Integrated Department of Immunology, University of Colorado School of Medicine and National Jewish Health , Denver, CO 80206"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2012,9,15]]},"reference":[{"key":"2025032409261010200_r1","doi-asserted-by":"crossref","first-page":"1097","DOI":"10.1172\/JCI200114235","article-title":"Mechanisms for the induction of autoimmunity by infectious agents","volume":"108","author":"Wucherpfennig","year":"2001","journal-title":"J. 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