Source:http://linkedlifedata.com/resource/pubmed/id/18641331
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2008-7-21
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pubmed:abstractText |
Several factors affect the autoimmune response, including iron-dependent modulation of T cells. Hemopexin is the plasma protein with the highest binding affinity to heme. It mediates heme-iron recovery in the liver, thus controlling heme-iron availability in peripheral cells. The aim of the present study was to investigate the role of hemopexin in the progress of an autoimmune response. To this end, we chose a mouse model of mercury-induced autoimmunity and evaluated the susceptibility of hemopexin-null mice to mercury treatment compared with wild-type controls. In this study we show that lack of hemopexin dampens mercury-induced autoimmune responses in mice. Hemopexin-null mice produced fewer antinuclear autoantibodies and had reduced deposits of immune complexes in the kidney after mercuric chloride treatment compared with wild-type mice. These features were associated with a reduction in activated T cells and lower absolute B cell number in spleen and impaired IgG1 and IgG2a production. In contrast, in hemopexin-null mice the response to OVA/CFA immunization was maintained. In addition, hemopexin-null mice had reduced transferrin receptor 1 expression in T cells, possibly due to the increase in heme-derived iron. Interestingly, CD4(+)T cells isolated from mercury-treated hemopexin-null mice show reduced IFN-gamma-dependent STAT1 phosphorylation compared with that of wild-type mice. Our data suggest that hemopexin, by controlling heme-iron availability in lymphocytes, modulates responsiveness to IFN-gamma and, hence, autoimmune responses.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1550-6606
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
181
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1937-47
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pubmed:meshHeading |
pubmed-meshheading:18641331-Animals,
pubmed-meshheading:18641331-Autoimmunity,
pubmed-meshheading:18641331-CD4-Positive T-Lymphocytes,
pubmed-meshheading:18641331-Cell Membrane Permeability,
pubmed-meshheading:18641331-Cytokines,
pubmed-meshheading:18641331-Hemopexin,
pubmed-meshheading:18641331-Mercuric Chloride,
pubmed-meshheading:18641331-Mice,
pubmed-meshheading:18641331-Mice, Knockout,
pubmed-meshheading:18641331-Microscopy, Electron, Transmission,
pubmed-meshheading:18641331-Organ Specificity,
pubmed-meshheading:18641331-Spleen
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pubmed:year |
2008
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pubmed:articleTitle |
Lack of plasma protein hemopexin dampens mercury-induced autoimmune response in mice.
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pubmed:affiliation |
Department of Genetics, Biology and Biochemistry, and Molecular Biotechnology Center, University of Turin, Turin, Italy. sharmila.fagoonee@unito.it
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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