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rdf:type |
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lifeskim:mentions |
umls-concept:C0021760,
umls-concept:C0024518,
umls-concept:C0035820,
umls-concept:C0040561,
umls-concept:C0040690,
umls-concept:C0041904,
umls-concept:C0162493,
umls-concept:C0205191,
umls-concept:C0205470,
umls-concept:C0456387,
umls-concept:C2603343
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pubmed:issue |
4
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pubmed:dateCreated |
2001-3-20
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pubmed:abstractText |
A murine model was used to characterize the local immune and inflammatory response during ocular toxoplasmosis. Major histocompatibility complex (MHC) class I, normally expressed at low levels in immune-privileged sites such as the eye, was up-regulated during infection as determined by competitive reverse transcriptase (RT)-PCR and immunocytochemistry for both beta2-microglobulin and the MHC class I heavy chain. However, the eyes of chronically infected mice also had increased levels of mRNA transcripts for transforming growth factor beta, a cytokine associated with immune privilege and constitutively expressed in normal eyes. Transcripts for a number of inflammatory mediators, including interleukin-6 (IL-6), were increased during chronic infection. The role of IL-6 was further investigated by comparing disease progression and the development of the local immune response in wild-type (WT) and IL-6-deficient mice (IL-6(-/-) mice). Following infection, IL-6(-/-) mice developed more severe inflammation in the retina and vitreous humor compared with WT mice. This increased severity of disease was associated with reduced ocular IL-1alpha and increased tumor necrosis factor alpha mRNA production compared with WT mice. Moreover, the increased severity of disease in IL-6(-/-) mice correlated with increased eye parasite burden as determined by RT-PCR for the Toxoplasma gondii bradyzoite-specific LDH2 gene. These results demonstrate alterations to components of immune privilege as a result of ocular toxoplasmosis and a role for IL-6 in controlling parasite numbers and inflammation in the eye.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11254623-10234186,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11254623-10603418,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/11254623-9651924
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0019-9567
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
69
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2589-95
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:11254623-Animals,
pubmed-meshheading:11254623-Chronic Disease,
pubmed-meshheading:11254623-Eye,
pubmed-meshheading:11254623-Female,
pubmed-meshheading:11254623-Gene Expression Regulation,
pubmed-meshheading:11254623-Histocompatibility Antigens Class I,
pubmed-meshheading:11254623-Immunohistochemistry,
pubmed-meshheading:11254623-Interleukin-6,
pubmed-meshheading:11254623-Mice,
pubmed-meshheading:11254623-Toxoplasma,
pubmed-meshheading:11254623-Toxoplasmosis, Ocular,
pubmed-meshheading:11254623-Transforming Growth Factor beta,
pubmed-meshheading:11254623-Up-Regulation,
pubmed-meshheading:11254623-beta 2-Microglobulin
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pubmed:year |
2001
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pubmed:articleTitle |
Immunological studies of chronic ocular toxoplasmosis: up-regulation of major histocompatibility complex class I and transforming growth factor beta and a protective role for interleukin-6.
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pubmed:affiliation |
Department of Immunology, Strathclyde Institute for Biomedical Sciences, University of Strathclyde, Glasgow, Scotland.
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pubmed:publicationType |
Journal Article
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