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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
1998-3-13
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pubmed:abstractText |
Fas antigen (Fas) is a cell surface receptor molecule that mediates apoptosis-inducing signals into activated and/or autoreactive peripheral T and B cells by stimulation with Fas ligand or agonistic anti-Fas mAb. The i.p. administration of the hamster anti-mouse Fas mAb RK-8, which induced apoptosis both in vivo and in vitro, did not kill adult mice, whereas those given another hamster anti-mouse Fas mAb Jo2 rapidly die of fulminant hepatitis with hemorrhage. Here, we report that MRL-gld/gld mice thoroughly recovered and/or were prevented from glomerulonephritis, arthritis, sialadenitis, vasculitis and lymphoadenopathy after receiving a single administration of the agonistic anti-mouse Fas mAb RK-8. The serum levels of autoantibodies were decreased after the administration. All the therapeutic effects of RK-8 persisted for >6 months. These findings suggest that the systemic administration of agonistic anti-Fas mAb without fulminant hepatitis-inducing activity is a useful therapeutic strategy for treating systemic autoimmune disease.
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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 |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/Autoantibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Fas Ligand Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Fasl protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tnfsf6 protein, rat
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0953-8178
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
9
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1793-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:9466307-Animals,
pubmed-meshheading:9466307-Antibodies, Monoclonal,
pubmed-meshheading:9466307-Antigens, CD95,
pubmed-meshheading:9466307-Apoptosis,
pubmed-meshheading:9466307-Arthritis, Experimental,
pubmed-meshheading:9466307-Autoantibodies,
pubmed-meshheading:9466307-Autoimmune Diseases,
pubmed-meshheading:9466307-B-Lymphocytes,
pubmed-meshheading:9466307-Cricetinae,
pubmed-meshheading:9466307-Fas Ligand Protein,
pubmed-meshheading:9466307-Female,
pubmed-meshheading:9466307-Glomerulonephritis,
pubmed-meshheading:9466307-Lung,
pubmed-meshheading:9466307-Lymphatic Diseases,
pubmed-meshheading:9466307-Lymphocyte Activation,
pubmed-meshheading:9466307-Membrane Glycoproteins,
pubmed-meshheading:9466307-Mice,
pubmed-meshheading:9466307-Mice, Inbred Strains,
pubmed-meshheading:9466307-Rats,
pubmed-meshheading:9466307-Salivary Glands,
pubmed-meshheading:9466307-Splenomegaly,
pubmed-meshheading:9466307-T-Lymphocytes
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pubmed:year |
1997
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pubmed:articleTitle |
Amelioration of systemic autoimmune disease by the stimulation of apoptosis-promoting receptor Fas with anti-Fas mAb.
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pubmed:affiliation |
The Pharmaceutical Basic Research Laboratories, JT Inc., Yokohama, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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