Previous studies involving animals have shown that parasite infection can influence the course of autoimmune diseases. These studies suggest that individuals with parasite infections have a diminished T cell response when unrelated antigens (foreign substances that generate an immune response) are present. The current study, conducted by Jorge Correale, M.D., and Mauricio Farez, B.Sc., of the Raúl Carrea Institute for Neurological Research in Buenos Aires, Argentina, involved 12 patients with MS who also had a parasite infection, 12 controls with MS who were uninfected, and 12 healthy individuals. The two groups of MS patients had a similar disease course. Patients had a neurological exam every three months and a brain MRI every 6 months, while immunological evaluations were conducted during the last 12 to 18 months of the study. Patients were followed for an average of 4.6 years.
During the study period, there were three clinical relapses of MS in the infected group and 56 relapses in the uninfected group. Only two infected patients showed minimal Expanded Disability Status Score changes (EDSS is used to measure disability due to MS) that lasted less than three months, while the other 10 had no changes in EDSS scores. In the uninfected group, 11 patients showed an overall increase in EDSS. Since MS involves an inflammatory response associated with the production of certain regulatory proteins known as cytokines, the number of cells producing cytokine suppressants was measured and found to be significantly higher in infected patients.
The authors suggest that their findings provide evidence to support that an autoimmune response as a result of parasite infection can result in a decrease in the normal inflammatory response associated with MS. They note that evidence for production of regulatory T cells (which inhibit the immune response) in parasite infection is now emerging, which offers an explanation for the mechanism by which infected hosts exhibit an altered immune response that affects a secondary antigen, as was the case in the current study. "Thus, parasites may lead to increased regulatory T cell numbers or activity, either by generating new cells or by activating/expanding existing cells," they state.
Because parasites inhabit their hosts for long periods of time, they can develop molecules that generate strong anti-inflammatory responses, which enhance their survival. Further investigation is warranted in order to identify which molecules cause immune system effects that dampen the inflammatory reactions normally seen in autoimmune diseases, the authors note. They conclude that "induction of a regulatory anti-inflammatory network generated by persistent parasite infections may offer a potential explanation for environment-related suppression of MS development in areas with low disease prevalence."