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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2006-1-20
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pubmed:abstractText |
Heat shock proteins (Hsp) are markedly up-regulated at sites of inflammation during autoimmune diseases like experimental autoimmune encephalomyelitis (EAE). In this study, we show that Hsp70-peptide complexes (pc) isolated from brains of mice with EAE prevented the development of EAE clinically and pathologically when administered before proteolipid protein 139-151 (PLP139-151) immunization. In contrast, pure Hsp70 or Hsp70-pc derived from brains of healthy mice or other inflamed tissue did not modulate the expression of EAE. In animals in which EAE had been suppressed by Hsp70-pc, lymphocytes showed increased cell death in response to PLP139-151 that correlated with elevated IFN-gamma and NO production. Coculture of spleen cells from Hsp70-pc immunized mice with spleen cells from untreated EAE mice, in addition to depletion experiments, showed that NK cells reduced reactivity to PLP139-151. Transfer of NK cells from Hsp70-pc-immunized mice to recipients sensitized for EAE abolished disease development. Thus, we propose that Hsp70 demonstrate the ability to bind to peptides generated during brain inflammation and to induce a regulatory NK cell population that is capable of preventing subsequent autoimmunization for EAE.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
176
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1588-99
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pubmed:dateRevised |
2011-8-26
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pubmed:meshHeading |
pubmed-meshheading:16424188-Animals,
pubmed-meshheading:16424188-Brain,
pubmed-meshheading:16424188-CD4-Positive T-Lymphocytes,
pubmed-meshheading:16424188-Cell Proliferation,
pubmed-meshheading:16424188-Cells, Cultured,
pubmed-meshheading:16424188-Coculture Techniques,
pubmed-meshheading:16424188-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:16424188-Female,
pubmed-meshheading:16424188-HSP70 Heat-Shock Proteins,
pubmed-meshheading:16424188-Immune Tolerance,
pubmed-meshheading:16424188-Immunotherapy, Adoptive,
pubmed-meshheading:16424188-Inflammation,
pubmed-meshheading:16424188-Interferon-gamma,
pubmed-meshheading:16424188-Interleukin-10,
pubmed-meshheading:16424188-Killer Cells, Natural,
pubmed-meshheading:16424188-Mice,
pubmed-meshheading:16424188-Mice, Inbred Strains,
pubmed-meshheading:16424188-Myelin Proteolipid Protein,
pubmed-meshheading:16424188-Nitric Oxide,
pubmed-meshheading:16424188-Peptide Fragments,
pubmed-meshheading:16424188-Peptides,
pubmed-meshheading:16424188-T-Lymphocytes,
pubmed-meshheading:16424188-Up-Regulation
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pubmed:year |
2006
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pubmed:articleTitle |
Brain-derived heat shock protein 70-peptide complexes induce NK cell-dependent tolerance to experimental autoimmune encephalomyelitis.
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pubmed:affiliation |
Department of Neurology, Medical University of Lodz, Lodz, Poland.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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