The role of chemokines in controlling granulomatous inflammation in Schistosoma mansoni infection
Chemokines are a superfamily of low-molecular-weight cytokines that were initially described for their chemoattractant activity. It is now clear chemokines have several other activities that modulate immune processes. Chemokines appear to play a role in the pathogenesis of several inflammatory disea...
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Published in | Acta tropica Vol. 108; no. 2; pp. 135 - 138 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Netherlands
Elsevier B.V
01.11.2008
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Subjects | |
Online Access | Get full text |
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Summary: | Chemokines are a superfamily of low-molecular-weight cytokines that were initially described for their chemoattractant activity. It is now clear chemokines have several other activities that modulate immune processes. Chemokines appear to play a role in the pathogenesis of several inflammatory diseases. The role of chemokines and their receptors in mediating granulomatous inflammation induced by
Schistosoma mansoni egg antigens presented in particulate manner have been studied in detail. Much less is known of the role of chemokines in mediating inflammation during the course of
S. mansoni infection. Our studies in mice suggest a relevant role for the chemokine CCL3 and the receptor CCR5 in the pathogenesis of experimental
S. mansoni infection. Absence of CCL3 is associated with decrease in granuloma size, fibrosis and parasite load. In humans, levels of CCL3 in plasma associate with disease severity and may be useful for diagnostic purposes. In contrast, absence of CCR5 is associated with enhanced lethality, granuloma size and fibrosis. It is suggested that the balance of chemokine production and chemokine receptor activation are important determinants of the fate of infection in experimental animals and humans. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 |
ISSN: | 0001-706X 1873-6254 |
DOI: | 10.1016/j.actatropica.2008.04.016 |