Inventors created the IL-1 beta deficient mouse strain by targeting the IL-1 beta gene in embryonic stem cells. These mice develop and grow normally. Endotoxin-stimulated peritoneal macrophages from IL-1beta- deficient mice showed normal synthesis and cellular release of IL- 1alpha after treatment with 5 mM ATP demonstrating that IL-1beta is not necessary for expression and release of the IL-1alpha isoform. Mice deficient in IL-1beta showed unaltered sensitivity to endotoxic shock, with or without pretreatment with D-galactosamine. In contrast, IL- 1beta-deficient mice showed defective contact hypersensitivity responses to topically applied trinitrochlorobenzene (TNCB).