A view that Th1/CD4 lymphocytes are responsible for inflammation in multiple sclerosis is very common. However, it was proved that destruction of the axons in the demyelination plaque correlated better with macrophages and CD4 lymphocytes activity than CD8 lymphocytes activity. Macrophages play a key role in all the multiple plaques. They are usually surrounded by lymphocytes and located around the small venous vessels. Macrophages undergo polarization that depends on the activating factors. In autoimmune disorders phenotype M1 of macrophages overbalance in acute phase of inflammation. Stimulation of PRR signaling path inducts M1 to produce inflammatory cytokine like No, ROIs that destroy the tissues, TNF-alfa, IL-beta that activate inflammatory signaling NF-kappaB, as well as IL-12 and IL-23 that induce Th1 response for antigens presented by macrophages. Cytokines with the most important one Il-17 promote inflammatory process. The latest research has pointed to a crucial role for microglia activated through TLRs in polarization of γδ T cells towards neurotoxic IL-17+ γδ T cells. We have screened a library of PubMed in order to identify M2 activating substances that could be used as the potential new medications for multiple sclerosis. Interestingly, we found one very promising recent research.
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