Cellular and humoral immunity to the 60-kD heat shock protein in inflammatory bowel disease.

Abstract

Mycobacteria have been considered a possible etiological agent in Crohn's disease. Since cross-reactivity between epitopes of mycobacterial and self-heat shock protein might represent a potential disease mechanism, we determined the cellular and humoral immune responses to the mycobacterial and the human 60-kD heat shock protein, as well as various control antigens. We studied samples from 19 patients with Crohn's disease, 12 patients with ulcerative colitis, and from 19 healthy individuals. T cell responses were studied using a standard proliferation assays to purified recombinant mycobacterial and human 60-kD heat shock protein. Antibody levels were measured by establishing an enzyme-linked immunosorbent assays to recombinant purified 60-kD heat shock protein. The proliferative responses to the mycobacterial and the human 60-kD heat shock protein were closely correlated, but the cellular immune response to both antigens was not significantly different between the two patient groups and healthy controls. In addition, antibody levels to heat shock protein were also not significantly different between the three groups. These results argue strongly against a role for mycobacterial heat shock protein in the pathogenesis of Crohn's disease. However, in view of previous data demonstrating overexpression of 60-kD heat shock protein in inflammatory Crohn's disease tissue, this considerable cellular and humoral autoreactivity suggests an important immunoregulatory role for the 60-kD heat shock protein.