Abstract
A synthetic peptide corresponding to 86–93 of the human type I IL-1 receptor and its analogues bound human recombinant (hr) IL-1 (α and β)and inhibited dose-dependently both Con A-stimulated proliferation of mouse spleen cells andhrIL-1β-stimulated formation of tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cells in rat bone marrow cell cultures. Furthermore, hrIL-1β-induced mouse paw edema was dose-dependently inhibited by systemic administration (ip) of the synthetic peptide. These results suggest that one of the IL-1 binding sites of the human type I IL-1 receptor comes to the region of 86–93 and the synthetic peptide having the ability to bind hrIL-1 (α and β) blocks the biological activities of exogenous hrIL-1β and endogenous mouse IL-1.
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