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Complement-dependent enhancement of CD8+ T cell immunity to lymphocytic choriomeningitis virus infection in decay-accelerating factor-deficient mice.
Fang, Chongyun; Miwa, Takashi; Shen, Hao; Song, Wen-Chao.
Afiliação
  • Fang C; Institute for Translational Medicine and Therapeutics and Department of Pharmacology, University of Pennsylvania School of Medicine, 421 Curie Boulevard, Philadelphia, PA 19104, USA.
J Immunol ; 179(5): 3178-86, 2007 Sep 01.
Article em En | MEDLINE | ID: mdl-17709533
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(-/-)) 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(-/-) mice also displayed significantly higher killing activity than cells from wild-type mice toward viral Ag-loaded target cells, and Daf-1(-/-) mice cleared LCMV more efficiently. Importantly, deletion of the complement protein C3 or the receptor for the anaphylatoxin C5a (C5aR) from Daf-1(-/-) 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.
Assuntos
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Base de dados: MEDLINE Assunto principal: Complemento C3 / Linfócitos T Citotóxicos / Complemento C5a / Antígenos CD55 / Coriomeningite Linfocítica / Vírus da Coriomeningite Linfocítica Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Ano de publicação: 2007 Tipo de documento: Article
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Base de dados: MEDLINE Assunto principal: Complemento C3 / Linfócitos T Citotóxicos / Complemento C5a / Antígenos CD55 / Coriomeningite Linfocítica / Vírus da Coriomeningite Linfocítica Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Ano de publicação: 2007 Tipo de documento: Article