Multiple sclerosis: peripheral mononuclear cells inhibit Plasmodium falciparum growth and are activated by parasite antigens.

The human genome has been subjected to selective pressures to resist to infectious agents in spite of a heavy segregational load. With this regard, thalassaemia and glucose-6-phosphate dehydrogenase deficiency have been considered an efficient genetic protection against P. falciparum malaria in Sardinia, insular Italy1,2. In this island, some multiple sclerosis (MS)-associated HLA haplotypes have the highest odds ratios in the same highestrate malarious areas of the island3. Moreover, tumor necrosis factor (TNF) polymorphisms epidemiologically associated with both MS and malaria are ten-fold more frequent amongst Sardinians compared to other populations worldwide4. A possible association between MS and malaria in this island was never analysed experimentally. We studied the immunological response of mononuclear cells to P. falciparum and the killing effect of macrophages on parasites in Sardinian MS patients and in matched healthy controls (HC).