Role of microglia in CNS autoimmunity

Abstract

Multiple sclerosis (MS) is the most common autoimmune disease of the central nervous system (CNS) in the Western world. The disease is characterized histologically by the infiltration of encephalitogenic TH1/TH17-polarized CD4(+) T cells, B cells, and a plethora of myeloid cells, resulting in severe demyelination ultimately leading to a degeneration of neuronal structures. These pathological processes are substantially modulated by microglia, the resident immune competent cells of the CNS. In this overview, we summarize the current knowledge regarding the highly diverse and complex function of microglia during CNS autoimmunity in either promoting tissue injury or tissue repair. Hence, understanding microglia involvement in MS offers new exciting paths for therapeutic intervention.

Figure 1

Polarization and function of activated microglia in CNS autoimmune inflammation. Microglia are activated by diverse stimuli, which define the polarization status of the cell. While IFN-γ/LPS promote the proinflammatory M1 status, IL-4/IL-10 or IL-13 induce the anti-inflammatory M2 status. M1 microglia take part in the attraction and differentiation of pathogenic T_H1/T_H17 T-cells, whereas M2 microglia promote phagocytosis of myelin debris, which is important for remyelination.