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Pelegrí, Carme; Kühnlein, Petra; Buchner, Eberhard; Schmidt, Carsten B.; Franch, Angels; Castell, Margarida; Hünig, Thomas; Emmrich, Frank; Kinne, Raimund W.
Arthritis and rheumatism, February 1996, Letnik: 39, Številka: 2Journal Article
Objective. To investigate the role of γ/δ T cells in Mycobacterium tuberculosis–induced rat adjuvant arthritis. Methods. Rats with adjuvant arthritis were injected with the anti–T cell receptor γ/δ (anti‐TCR γ/δ) monoclonal antibody V65 according to a preventive protocol, a pre–arthritis peak protocol, and a late therapeutic protocol. Arthritis severity and joint destruction were monitored, and depletion of target cells was analyzed by flow cytometry. Results. Although all protocols led to successful depletion of TCRγ/δbright cells in peripheral blood and lymph nodes, none of the regimens influenced clinical parameters of adjuvant arthritis. If rats were treated before the clinical peak of adjuvant arthritis, however, joint destruction was significantly more severe than in vehicle‐treated rats. Conclusion. Rat adjuvant arthritis is not promoted or perpetuated by γ/δ T cells. Aggravation of joint destruction with pre–arthritis peak anti‐γ/δ treatment suggests a stage‐dependent protective role of γ/δ T cells in adjuvant arthritis.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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in: SICRIS
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