{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T10:58:30Z","timestamp":1790247510488,"version":"4.1.0"},"reference-count":44,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2007,9,1]],"date-time":"2007-09-01T00:00:00Z","timestamp":1188604800000},"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":[[2007,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Decay-accelerating factor (DAF, CD55) is a GPI-anchored membrane protein that regulates complement activation on autologous cells. In addition to protecting host tissues from complement attack, DAF has been shown to inhibit CD4+ T cell immunity in the setting of model Ag immunization. However, whether DAF regulates natural T cell immune response during pathogenic infection is not known. We describe in this study a striking regulatory effect of DAF on the CD8+ T cell response to lymphocytic choriomeningitis virus (LCMV) infection. Compared with wild-type mice, DAF knockout (Daf-1\u2212\/\u2212) mice had markedly increased expansion in the spleen of total and viral Ag-specific CD8+ T cells after acute or chronic LCMV infection. Splenocytes from LCMV-infected Daf-1\u2212\/\u2212 mice also displayed significantly higher killing activity than cells from wild-type mice toward viral Ag-loaded target cells, and Daf-1\u2212\/\u2212 mice cleared LCMV more efficiently. Importantly, deletion of the complement protein C3 or the receptor for the anaphylatoxin C5a (C5aR) from Daf-1\u2212\/\u2212 mice reversed the enhanced CD8+ T cell immunity phenotype. These results demonstrate that DAF is an important regulator of CD8+ T cell immunity in viral infection and that it fulfills this role by acting as a complement inhibitor to prevent virus-triggered complement activation and C5aR signaling. This mode of action of DAF contrasts with that of CD59 in viral infection and suggests that GPI-anchored membrane complement inhibitors can regulate T cell immunity to viral infection via either a complement-dependent or -independent mechanism.<\/jats:p>","DOI":"10.4049\/jimmunol.179.5.3178","type":"journal-article","created":{"date-parts":[[2014,4,18]],"date-time":"2014-04-18T19:17:46Z","timestamp":1397848666000},"page":"3178-3186","source":"Crossref","is-referenced-by-count":51,"title":["Complement-Dependent Enhancement of CD8+ T Cell Immunity to Lymphocytic Choriomeningitis Virus Infection in Decay-Accelerating Factor-Deficient Mice"],"prefix":"10.1093","volume":"179","author":[{"given":"Chongyun","family":"Fang","sequence":"first","affiliation":[{"name":"Institute for Translational Medicine and Therapeutics and Department of Pharmacology, University of Pennsylvania School of Medicine , Philadelphia, PA 1910"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Takashi","family":"Miwa","sequence":"additional","affiliation":[{"name":"Institute for Translational Medicine and Therapeutics and Department of Pharmacology, University of Pennsylvania School of Medicine , Philadelphia, PA 1910"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hao","family":"Shen","sequence":"additional","affiliation":[{"name":"Department of Microbiology, University of Pennsylvania School of Medicine , Philadelphia, PA 19104"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wen-Chao","family":"Song","sequence":"additional","affiliation":[{"name":"Institute for Translational Medicine and Therapeutics and Department of Pharmacology, University of Pennsylvania School of Medicine , Philadelphia, PA 1910"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2007,9,1]]},"reference":[{"key":"2026012809262460500_R1","first-page":"35","volume-title":"Annu. 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