{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T03:35:38Z","timestamp":1770089738083,"version":"3.49.0"},"reference-count":46,"publisher":"Oxford University Press (OUP)","issue":"9","license":[{"start":{"date-parts":[[2003,11,1]],"date-time":"2003-11-01T00:00:00Z","timestamp":1067644800000},"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":[[2003,11,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>In this study, we investigate the state of T cell-mediated immunity in B cell-deficient (B\u2212\/\u2212) mice infected with two strains of lymphocytic choriomeningitis virus known to differ markedly in their capacity to persist. In B\u2212\/\u2212 C57BL mice infected with the more persisting virus, virus-specific CD8+ T cells are initially generated that are qualitatively similar to those in wild-type mice. However, although cell numbers are well sustained over time, the capacity to produce cytokines is rapidly impaired. In similarly infected B\u2212\/\u2212 BALB\/c mice, virus-specific CD8+ T cells are completely deleted, indicating that host genotype influences the severity of the T cell defect. In B\u2212\/\u2212 C57BL mice infected with the less persisting virus, CD8+ T cell dysfunction was not as pronounced, although it was clearly present. Most importantly, the appearance of dysfunctional CD8+ T cells clearly precedes recrudescence of detectable virus, indicating that the T cell defect is not simply a secondary event due to virus buildup resulting from the failure of B\u2212\/\u2212 mice to produce neutralizing Abs. In contrast with CD8+ T cells, which initially respond almost as in wild-type mice, the priming of virus-specific CD4+ T cells was markedly impaired in B\u2212\/\u2212 mice infected with either virus strain. Thus, our results indicate that B cells play an important role in antiviral immunity not only as Ab producers, but also in promoting an optimal and sustained T cell response. The T cell defects are likely to contribute to the chronic course of viral infection in B\u2212\/\u2212 mice.<\/jats:p>","DOI":"10.4049\/jimmunol.171.9.4733","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T20:52:48Z","timestamp":1398027168000},"page":"4733-4741","source":"Crossref","is-referenced-by-count":39,"title":["Deficient CD4+ T Cell Priming and Regression of CD8+ T Cell Functionality in Virus-Infected Mice Lacking a Normal B Cell Compartment"],"prefix":"10.1093","volume":"171","author":[{"given":"Jan Pravsgaard","family":"Christensen","sequence":"first","affiliation":[{"name":"Institute of Medical Microbiology and Immunology, University of Copenhagen , Copenhagen ,","place":["Denmark"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Susanne \u00d8rding","family":"Kauffmann","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology and Immunology, University of Copenhagen , Copenhagen ,","place":["Denmark"]}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Allan Randrup","family":"Thomsen","sequence":"additional","affiliation":[{"name":"Institute of Medical Microbiology and Immunology, University of Copenhagen , Copenhagen ,","place":["Denmark"]}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2003,11,1]]},"reference":[{"key":"2026020210202663900_R1","first-page":"1365","volume-title":"J. 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