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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
1991-6-6
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pubmed:abstractText |
Recent experimental and clinical data point to the T helper lymphocyte subset as playing a central role in the pathogenesis of rheumatoid arthritis (RA). Thus, a therapeutic strategy aimed specifically at the CD4 T cell subset is warranted. We treated patients with active RA for 7 days with a daily dose of 20 mg of CD4 monoclonal antibody M-T151, administered intravenously over 30 minutes. There were no negative side effects. According to changes in the combined parameters of Ritchie articular index, pain assessment, grip strength, and morning stiffness, 6 patients had a good response. Clinical improvement was greatest approximately 2 weeks after termination of the therapy and lasted from 4 weeks to 6 months. Of the serologic parameters of inflammation, only the C-reactive protein level improved in the patients with a favorable response. Close immunologic monitoring revealed a transient, selective depletion of CD4+ T cells after each infusion. During the entire treatment period, residual circulating CD4+ cells were found to be coated with CD4 antibody, whereas free antibody was detected in the serum only for approximately 8 hours after each infusion. Immediately after infusion, soluble CD4 antigen appeared in the serum. In addition to the cell-bound CD4 antibody, complement components could be detected on the surface of the remaining CD4+ cells. The proliferative response of peripheral blood mononuclear cells to purified protein derivative was significantly diminished 4 weeks after cessation of antibody treatment. Six patients showed a weak antibody response to mouse immunoglobulin. In 4 of the responders who received a second course of therapy (2 of them as outpatients), a therapeutic effect was noted that was similar to that after the first course. Only 1 patient, who had low titers of serum IgE anti-mouse Ig antibodies, showed a mild anaphylactic reaction at the end of the second course of therapy. Treatment of RA with the monoclonal CD4 antibody M-T151 seems to be a promising alternative, although the optimal dose and the regimen of administration are still to be defined.
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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 |
May
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pubmed:issn |
0004-3591
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
34
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
525-36
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:2025306-Animals,
pubmed-meshheading:2025306-Antibodies, Anti-Idiotypic,
pubmed-meshheading:2025306-Antibodies, Monoclonal,
pubmed-meshheading:2025306-Antigens, CD4,
pubmed-meshheading:2025306-Arthritis, Rheumatoid,
pubmed-meshheading:2025306-Cell Division,
pubmed-meshheading:2025306-Complement Activation,
pubmed-meshheading:2025306-Follow-Up Studies,
pubmed-meshheading:2025306-Humans,
pubmed-meshheading:2025306-Immunoglobulins,
pubmed-meshheading:2025306-Lymphocyte Subsets,
pubmed-meshheading:2025306-Mice,
pubmed-meshheading:2025306-Solubility
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pubmed:year |
1991
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pubmed:articleTitle |
Treatment of rheumatoid arthritis with monoclonal CD4 antibody M-T151. Clinical results and immunopharmacologic effects in an open study, including repeated administration.
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pubmed:affiliation |
Institute for Immunology, University of Munich, Germany.
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pubmed:publicationType |
Journal Article
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