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- Title
Immunopathology of thrombocytopenia in experimental malaria.
- Authors
Grau, G. E.; Piguet, P. -F.; Gretener, D.; Vesin, C.; Lambert, P. H.
- Abstract
An early thrombocytopenia was observed in CBA mice during acute infection with Plasinodium berghei. This was associated with an increase in bone marrow megakaryocytes and a reduction of normal syngeneic 111Indium-labelled platelet life span. Malaria-induced thrombocytopenia was thus considered to be the result of increased peripheral platelet destruction rather than central hypoproduction. The occurrence of thrombocytopenia was modulated by T-cell depletion. Indeed, thymectomized, irradiated or anti-CD4 monoclonal antibody-treated mice failed to develop thrombocytopenia, although they were infected to the same extent. Conversely, a significant thrombocytopenia was observed in thymectomized mice reconstituted with CD4+ T cells. During the course of infection, a significant inverse correlation was found between platelet counts and plateletapsociated IgG. Normal mice passively transfered with serum from syngeneic malaria-infected mice developed thrombocytopenia. The possibility to raise monoclonal anti-platelet antibodies from P. berghei-infected animals further suggested a role for an antibody-mediated platelet destruction during acute murine malaria infection. These results indicate that in murine malaria, thrombocytopenia is mediated by immune mechanisms and that CD4+ T cells might be significantly involved.
- Subjects
THROMBOCYTOPENIA; MALARIA; IMMUNOPATHOLOGY; CLINICAL immunology; BLOOD platelet disorders; PROTOZOAN diseases
- Publication
Immunology, 1988, Vol 65, Issue 4, p501
- ISSN
0019-2805
- Publication type
Article