Why does multiple sclerosis only affect humans?

1 July 2015

BPRC - 1. Why does multiple sclerosis only affect humans?

Multiple sclerosis (MS) develops exclusively in humans. Non-human primates are resistant against MS, although they seem to be highly susceptible to experimentally induced MS-like disease. Unraveling of the cause(s) underlying this discrepancy is highly relevant as insights might be gained into the elusive event(s) that trigger(s) MS.

A well-established difference between humans and non-human primates is that humans are unable to synthesize a certain sugar, the sialic acid N-glycolylneuraminic acid (Neu5Gc). However, Neu5Gc can be found in the human body as a result of long-term red meat consumption. In a BPRC publication in the MS Journal (http://msj.sagepub.com/content/early/recent), it is proposed that the presence of foreign Neu5Gc in the human body may lead to a detrimental immune attack that can initiate MS. Therefore long-term red meat consumption may be an ignored environmental risk factor for MS.

Validation of this concept may be possible in marmosets, since they have the same genetic defect for Neu5Gc and share similar MS-like autoimmune reactions. In another paper authored by a BPRC researcher (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4435712/), the relevance of non-human primate (marmoset) research for MS is elaborated. The article explains that these models are unique because, similar to humans, a mature immune system attacks the own body (autoimmune response), resulting in neurological disease.

Maturity is induced by the daily combat with environmental pathogens and with chronic latent infection by pathogens. The need to suppress exacerbation of the infections creates a repertoire of highly reactive immune cells, which may give rise to autoimmune responses. This pathogen-educated immune system is absent in rodents that are raised under semi-sterile laboratory conditions. The (marmoset)monkey-MS model can therefore provide relevant information on the still poorly understood relation between infection and autoimmunity.