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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
7
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pubmed:dateCreated |
1994-10-14
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pubmed:abstractText |
Autoimmune diseases can be characterized by increases in Th cell activities, suggesting that inhibition of Th cell function might ameliorate autoimmunity. We have recently reported that administration of nonmitogenic anti-CD3 mAb (nmCD3) to nonautoimmune mice can induce long-term Th cell hyporesponsiveness, reflected by reduced IL-2 secretion upon re-exposure to Ag. This study was designed to determine the effects of nmCD3 on autoimmunity by using the murine collagen-induced arthritis model. Treatment of DBA/1 mice with nmCD3 delayed the onset and reduced the severity of arthritis in mice immunized with type II collagen (CII). This effect was not caused by depletion of T cells or modulation of TCR. The observed inhibition of arthritis was not caused by decreased Ab production, as anti-CII titers were not affected. Rather, lymph node cells from CII-immunized mice treated with nmCD3 were hyporesponsive to in vitro stimulation with CII. This hyporesponsiveness was reflected by a marked decrease in secretion of IL-2 and IFN-gamma, but not of IL-4, which suggests that nmCD3 had its principal effect on Th1 cells. The hyporesponsiveness was not Ag-specific, because IL-2 and IFN-gamma production in response to a pan-T cell mitogen was also reduced. These results demonstrate that induction of Th1 cell hyporesponsiveness with nmCD3 can significantly alter the course of CIA and suggest that IL-2 and/or IFN-gamma play a crucial role in disease pathogenesis.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Collagen,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
153
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3319-25
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8089501-Animals,
pubmed-meshheading:8089501-Antibodies, Monoclonal,
pubmed-meshheading:8089501-Antibody Formation,
pubmed-meshheading:8089501-Antigens, CD3,
pubmed-meshheading:8089501-Arthritis,
pubmed-meshheading:8089501-Autoimmunity,
pubmed-meshheading:8089501-Collagen,
pubmed-meshheading:8089501-Cytokines,
pubmed-meshheading:8089501-Lymphocyte Activation,
pubmed-meshheading:8089501-Male,
pubmed-meshheading:8089501-Mice,
pubmed-meshheading:8089501-Mice, Inbred DBA,
pubmed-meshheading:8089501-Receptors, Antigen, T-Cell,
pubmed-meshheading:8089501-T-Lymphocyte Subsets,
pubmed-meshheading:8089501-T-Lymphocytes, Helper-Inducer
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pubmed:year |
1994
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pubmed:articleTitle |
Induction of T helper cell hyporesponsiveness in an experimental model of autoimmunity by using nonmitogenic anti-CD3 monoclonal antibody.
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pubmed:affiliation |
Division of Rheumatology, Children's Hospital Medical Center, University of Cincinnati, OH 45229.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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