Histopathological and immunohistochemical study of type 3 complement receptors (CD11b/CD18) in livers and spleens of asymptomatic and symptomatic dogs naturally infected with Leishmania ( Leishmania) chagasi
Leishmania promastigotes interact with macrophages through the association of multiple membrane surface receptors. Macrophage complement receptor CR3 (CD11b/CD18 or Mac-1) has been implicated in the interaction of both human and murine macrophages with serum-opsonized promastigotes. The aim of this...
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Published in: | Veterinary Immunology and Immunopathology Vol. 117; no. 1; pp. 129 - 136 |
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Main Authors: | , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Netherlands
Elsevier B.V
15-05-2007
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Subjects: | |
Online Access: | Get full text |
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Summary: | Leishmania promastigotes interact with macrophages through the association of multiple membrane surface receptors. Macrophage complement receptor CR3 (CD11b/CD18 or Mac-1) has been implicated in the interaction of both human and murine macrophages with serum-opsonized promastigotes. The aim of this study was to determine CR3 expression in the livers and spleens of dogs naturally infected with
Leishmania (
Leishmania)
chagasi.
CR3 expression in liver was higher in asymptomatic than in symptomatic animals. Moreover, the hepatic parasitism load determined by immunocytochemical analysis was lower in parallel with higher numbers of granulomas. In contrast, in spleens, CR3 expression was higher in symptomatic animals than in asymptomatic ones. However, the tissue parasite load was greater in spleens of symptomatic dogs. There was a strict correlation between the parasite load and cellular CR3 expression in the spleens of dogs naturally infected with
L. chagasi.
CR3 macrophage integrins could be essential receptors for
Leishmania survival. Considering that the symptomatic animals showed higher parasite loads and higher CD11b/CD18 expression in their spleens, we can conclude that these splenic cells (monocyte-macrophages) might serve to perpetuate intracellular infection. |
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Bibliography: | http://dx.doi.org/10.1016/j.vetimm.2007.02.012 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0165-2427 1873-2534 1365-2567 |
DOI: | 10.1016/j.vetimm.2007.02.012 |