Promoting the development and inflammatory lesions in CNS in the early stage of EAE
Eliminating debris and suppressing cellular metabolism at EAE onset Secretion of TGF-β to induce a protective process
Presenting antigen Activating myelin-reactive T cells Expressing adhesion molecules and chemokines to attract leukocyte infiltration into CNS Activating some microglia to accelerate inflammation
Contributing to the establishment of early inflammation in EAE Associating with EAE severity
Promoting the differentiation of Th2 cells and Tregs to suppress EAE severity Inhibiting the development of Th17 cells