Responses mediated by the immune system to antigenic challenge are considered to play a major role in the pathogenesis of certain inflammatory diseases. Murine investigations have revealed that immune response (Ir) genes exist that govern these reactions. For example, under experimental conditions, immunity to cartilage (type II) collagen can create connective tissue inflammation in rats and mice.1 The ability of this immunization protocol to induce inflammatory arthritis in squirrel monkeys2 has recently heightened interest in the possible relevance of this model for human disease.3 In rodents, both susceptibility to collagen arthritis and the immune response to this structural protein are linked to the murine equivalent of the human major histocompatibility locus, ie, the HLA-D region.
The genetic elements involved in immunologic recognition and response provide positive signals. The elucidation of Ir gene control for antigens in humans has been a more difficult task. This problem may, in
Trentham DE. Adverse Reactions to Bovine Collagen Implants: Additional Evidence for Immune Response Gene Control of Collagen Reactivity in Humans. Arch Dermatol. 1986;122(6):643–644. doi:10.1001/archderm.1986.01660180049011
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