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To address these issues, we have investigated the role of tumor necrosis factor receptors (TNFRs) I (p55R) and II (p75R) in regulating CD8 T-cell responses to lymphocytic choriomeningitis virus (LCMV) with wild-type, p55R-deficient (p55<jats:sup>\u2212\/\u2212<\/jats:sup>), p75R-deficient (p75<jats:sup>\u2212\/\u2212<\/jats:sup>), and p55R- and p75R-deficient (DKO) mice. Loss of p55R increased the number of memory CD8 T cells to only one of the two immunodominant epitopes, and p75R deficiency had a minimal impact on the T-cell response to LCMV. Strikingly, deficiency of both p55R and p75R had a more dramatic effect on the LCMV-specific CD8 T-cell response; in the DKO mice, as a sequel to enhanced expansion and a reduction in contraction of CD8 T cells, there was a substantial increase in the number of memory CD8 T cells (specific to the two immunodominant epitopes). While the majority of LCMV-specific memory CD8 T cells in wild-type mice were CD62L<jats:sup>hi<\/jats:sup>CCR7<jats:sup>hi<\/jats:sup>(central memory), a major proportion of memory CD8 T cells in DKO mice were CD62L<jats:sup>lo<\/jats:sup>CCR7<jats:sup>hi<\/jats:sup>. TNFR deficiency did not affect the proliferative renewal of memory CD8 T cells. Taken together, these data suggested that TNFRs p55R and p75R have overlapping roles in downregulating CD8 T-cell responses and establishment of immune homeostasis during an acute viral infection.<\/jats:p>","DOI":"10.1128\/jvi.79.1.202-213.2005","type":"journal-article","created":{"date-parts":[[2004,12,16]],"date-time":"2004-12-16T03:52:43Z","timestamp":1103169163000},"page":"202-213","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":55,"title":["Role of Tumor Necrosis Factor Receptors in Regulating CD8 T-Cell Responses during Acute Lymphocytic Choriomeningitis Virus Infection"],"prefix":"10.1128","volume":"79","author":[{"given":"M.","family":"Suresh","sequence":"first","affiliation":[{"name":"Department of Pathobiological Sciences, University of Wisconsin-Madison, Madison, Wisconsin"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anju","family":"Singh","sequence":"additional","affiliation":[{"name":"Department of Pathobiological Sciences, University of Wisconsin-Madison, Madison, Wisconsin"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher","family":"Fischer","sequence":"additional","affiliation":[{"name":"Department of Pathobiological Sciences, University of Wisconsin-Madison, Madison, Wisconsin"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","first-page":"521","volume":"160","year":"1984","unstructured":"Ahmed, R., A. 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