Abstract
Inflammatory reaction in multiple sclerosis is induced by the presence of endogenous danger signals caused by both pathogen danger patterns and locally formed altered self structures in brain tissue. Danger signals are identified by the set of PRR receptors expressed on innate immunity cells.
Inflammasomes and intracellular signaling pathways are induced in response to danger signals recognition followed by the production of proinflammatory mediators and presentation of antigens to autoreactive T cells. The harm effects in multiple sclerosis are associated with Th17 and Th1 subsets activities.
In contrary, Treg and Tr subsets are alleviating inflammatory response and their activity is enhanced by therapy. Both injury and reparation in multiple sclerosis are influenced by abnormal cell death, such as necrosis apoptosis and autophagy.