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Immunotherapy of collagen-induced arthritis by a T-cell antiproliferative molecule
D J Spannaus-Martin1, R Holmdahl, T F Kresina
1Department of Medicine, Miriam Hospital, Providence, Rhode Island 02906.
Abstract:
The present study describes a novel experimental immunotherapeutic methodology for the reduction of inflammatory synovitis that is noted in an animal model of rheumatoid arthritis. The reduction in inflammation is noted in the animals administered a contra-interleukin-2 (IL-2) cytokine secreted by a cloned T-cell line. The mechanism of reduction of inflammation by this cytokine is through the inhibition of activation and differentiation of T lymphocytes. The cytokine inhibits the in vitro mitogen activation of T-cell lymphocytes as well as antigen-specific activation of a collagen type II specific T-cell line. In addition, decreased levels of messenger RNA coding for interleukin-2 are noted in T lymphocytes and IL-2 activation of the collagen type II specific cell line is inhibited by the contra-IL-2 cytokine. This initial description of a reduction in inflammation by a contra-IL-2 lymphokine suggests that immunoregulatory biologic molecules that are antagonists to IL-2 may be useful for the experimental immunotherapy of cartilage connective tissue pathology.