Abstract |
Lewis rats experimentally infected with Yersinia enterocolitica develop sterile arthritis similar to Yersinia-associated reactive arthritis in humans. To investigate the putative role of alpha beta T cells in the pathogenesis of Yersinia-induced arthritis (YIA) rats were treated with the monoclonal antibody (mAb) R73 mAb directed against the rat alpha beta T cell receptor. In spite of reduction of alpha beta T cells in peripheral blood and in liver lesions of Yersinia-infected rats this serotherapy had no suppressive effect on YIA. Moreover, R73 mAb treatment had no influence on the number of alpha beta T cells in the inflammed synovial tissue. In contrast, R73 mAb serotherapy in Mycobaterium tuberculosis-immunized rats blocked development of adjuvant arthritis (AA) and suppressed the presence of alpha beta T cells in the synovial tissue. These results suggest fundamental differences between the immunopatho-mechanism of YIA caused by bacterial infection and AA induced by bacterial immunization and known to be T cell mediated. These data might have consequences for putative serotherapy of arthritis in humans.
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Authors | K Gaede, M Nazet, D Bosse, Hünig, J Heesemann |
Journal | Clinical immunology and immunopathology
(Clin Immunol Immunopathol)
Vol. 77
Issue 3
Pg. 339-48
(Dec 1995)
ISSN: 0090-1229 [Print] United States |
PMID | 7586745
(Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antibodies, Monoclonal
- Receptors, Antigen, T-Cell, alpha-beta
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Topics |
- Animals
- Antibodies, Monoclonal
(immunology, therapeutic use)
- Arthritis, Experimental
(therapy)
- Arthritis, Infectious
(etiology, therapy)
- Liver
(pathology)
- Male
- Rats
- Rats, Inbred Lew
- Receptors, Antigen, T-Cell, alpha-beta
(immunology)
- Specific Pathogen-Free Organisms
- Spleen
(pathology)
- Synovial Membrane
(pathology)
- T-Lymphocytes
(immunology)
- Tarsus, Animal
(pathology)
- Yersinia Infections
(etiology, therapy)
- Yersinia enterocolitica
(pathogenicity)
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