Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 105, Issue 2, Pages 629-634Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0711200105
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Funding
- NCI NIH HHS [CA40489, R37 CA040489, R01 CA040489] Funding Source: Medline
- NHLBI NIH HHS [HL42846, P01 HL031950, P01 HL078784, HL78784, HL31950, R37 HL042846, R01 HL042846] Funding Source: Medline
- NIAID NIH HHS [AI40696, R01 AI040696] Funding Source: Medline
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We found that mice infected with different isolates of lymphocytic choriomeningitis virus (LCMV) develop a mild hemorrhagic anemia, which becomes severe and eventually lethal in animals depleted of platelets or lacking integrin beta 3. Lethal hemorrhagic anemia is mediated by virus-induced IFN-alpha/beta that causes platelet dysfunction, mucocutaneous blood loss and suppression of erythropoiesis. in addition to the life-threatening hemorrhagic anemia, platelet-depleted mice fail to mount an efficient cytotoxic T lymphocyte (CTL) response and cannot clear LCMV. Transfusion of functional platelets into these animals reduces hemorrhage, prevents death and restores CTL-induced viral clearance in a manner partially dependent on CD40 ligand (CD40L). These results indicate that, upon activation, platelets expressing integrin 03 and CD40L are required for protecting the host against the induction of an IFN-alpha/beta-dependent lethal hemorrhagic diathesis and for clearing LCMV infection through CTLs.
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