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Suppression of experimental systemic lupus erythematosus (SLE) in mice via TNF inhibition by an anti-TNF monoclonal antibody and by pentoxiphylline

Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel; Shmuel Harofeh Geriatric Medical Center, Beer Yacov, Israel

M Dayan

H Zinger

E Mozes

Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel

We have previously shown that the clinical manifestations of experimental systemic lupus erythematosus (SLE) correlate with an early increased secretion of TNF and IL-1. In the present study, we examined the efficacy of two therapeutic modalities which lower TNF production or activity, on the clinical manifestations of the disease. Experimental SLE was induced in naive C3H.SW mice by injection of the human anti-DNA monoclonal antibody (mAb) bearing the common idiotype, 16/6 Id. Two weeks after booster injections, treatment with either an anti-TNF mAb, or pentoxiphylline (PTX) was started, for a period of 6 weeks. Production of TNF (by splenocytes) and IL-1 (by peritoneal macrophages) was determined 3 and 7 months after disease induction. The experimental mice were also followed for disease manifestations. Both treatment protocols, with anti-TNF mAb and with PTX, reduced the production of the two pro-inflammatory cytokines, TNF and IL-1, in mice with experimental SLE. Anti-DNA antibodies were significantly lower in the mice treated with either protocol. In addition, a significantly lower rate of leukopenia, proteinuria and immune complex deposition was observed in treated mice. Abrogation of TNF and IL-1 production in the early stages of experimental SLE by an anti-TNF mAb or by PTX improves the clinical status of mice affiicted with this autoimmune disease.

Key Words: anti TNF • experimental SLE

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