Source:http://linkedlifedata.com/resource/pubmed/id/18021365
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2007-11-20
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pubmed:abstractText |
The resolution from leishmanial infection is dependent on the coordinated interactions between the components of the cell mediated immune system and the activation of T-cell population into appropriate cytokine production and the activation of macrophages. Earlier reports established that C-C chemokines particularly macrophage inflammatory protein (MIP)-1alpha and macrophage chemoattractant protein (MCP)-1 restrict the parasitic burden via the regulation of impaired protein kinase C (PKC) signalling and induction of free-radical generation in murine leishmaniasis. This study explored the role of MIP-1alpha and MCP-1 in the induction of T helper 1 (Th1) immune response and suppression of T helper 2 (Th2) response in Leishmania donovani-infected BALB/c mice. These chemokines induced the known pro-inflammatory cytokine interleukin (IL)-12 secretion and inhibited the secretion of anti-inflammatory cytokines IL-10 and transforming growth factor-beta in infected macrophages. Impaired antigen presentation capability of infected macrophages was also restored by the chemokine treatment. C-C chemokine treatment resulted in reduced levels of mRNA expression of IL-10, but increased levels of mRNA expression of IL-12p40, interferon (IFN)-gamma, tumour necrosis factor-alpha and inducible nitric oxide synthase in both liver mononuclear cells as well as in splenocytes, reflecting a switch of CD4+ differentiation from Th2 to Th1. Flow cytometric analysis of infected spleen cells suggested that C-C chemokine treatment enhances the CD4+ T cells to produce increased levels of IFN-gamma. These studies hypothesize a promising immuno-prophylactic effect of chemokines against leishmaniasis by induction of Th1 cytokine release imparting a long-term resistance.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CCL2 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL3,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokines,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1365-3083
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
66
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
671-83
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pubmed:meshHeading |
pubmed-meshheading:18021365-Animals,
pubmed-meshheading:18021365-Cell Communication,
pubmed-meshheading:18021365-Cell Differentiation,
pubmed-meshheading:18021365-Chemokine CCL2,
pubmed-meshheading:18021365-Chemokine CCL3,
pubmed-meshheading:18021365-Chemokines,
pubmed-meshheading:18021365-Cricetinae,
pubmed-meshheading:18021365-Flow Cytometry,
pubmed-meshheading:18021365-Host-Parasite Interactions,
pubmed-meshheading:18021365-Leishmania donovani,
pubmed-meshheading:18021365-Leishmaniasis, Visceral,
pubmed-meshheading:18021365-Mice,
pubmed-meshheading:18021365-Mice, Inbred BALB C,
pubmed-meshheading:18021365-RNA, Messenger,
pubmed-meshheading:18021365-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:18021365-Th1 Cells,
pubmed-meshheading:18021365-Th2 Cells
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pubmed:year |
2007
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pubmed:articleTitle |
Induction of host protective Th1 immune response by chemokines in Leishmania donovani-infected BALB/c mice.
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pubmed:affiliation |
Department of Microbiology, Bose Institute, Kolkata, India.
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pubmed:publicationType |
Journal Article
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