T-cell responses to mycobacterial heat shock protein 60 (M.hsp60) have been implicated in the pathogenesis of adjuvant arthritis, but whether they play a role in rheumatoid arthritis (RA) is undefined. We therefore examined T-cell responses to M.hsp60 and to other recall antigens in a cohort of patients with early RA and in healthy controls.
In vitro peripheral blood mononuclear cells' (PBMC) proliferative responses to antigen were measured by [3H]thymidine incorporation, and results correlated with clinical and laboratory features of disease.
Whereas responses to the recall antigens tetanus toxin and purified protein derivative (PPD) were equivalent in the two groups, responses to both M.hsp60 and the Escherichia coli hsp60 were lower in the RA patients. These results could not be explained by either the higher prevalence of HLA-DR4 in the RA group, or the disease severity of the patients.
In the light of results from the adjuvant arthritis model which suggest that arthritis may be ameliorated by the actions of an hsp60-reactive T-cell population, the lack of response to M.hsp60 in RA could contribute to disease persistence.