Autor: |
Gaede, Karoline, Nazet, Martina, Bosse, Dietrich, Hünig, Thomas, Heesemann, Jürgen |
Zdroj: |
Clinical Immunology and Immunopathology (Now Called Clinical Immunology); December 1995, Vol. 77 Issue: 3 p339-348, 10p |
Abstrakt: |
Lewis rats experimentally infected with Yersinia enterocolitica develop sterile arthritis similar to Yersinia-associated reactive arthritis in humans. To investigate the putative role of αβ T cells in the pathogenesis of Yersinia-induced arthritis (YIA) rats were treated with the monoclonal antibody (mAb) R73 mAb directed against the rat αβ T cell receptor. In spite of reduction of αβ 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 αβ 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 αβ 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. Copyright 1995, 1999 Academic Press |
Databáze: |
Supplemental Index |
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