Figure 2.

The pathologic role of TCR, BCR and TH17-induced MALT-1 in demyelination and the inhibition of this signaling pathway by A20. As depicted in Figure 2, downstream of CBM, IKK complex is activated by MALT-1 that in turn, plays an essential role in the development of EAE-mediated Demyelination. MALT1, in other hand, cleaves the NF-κB inhibitory proteins A20 and CYLD as well as the NF-κB subunit RelB in antigen receptor-stimulated T cells and during EAE, suggesting a contribution of MALT1 proteolytic activity in T cell activation and EAE development. A20, negatively regulates TCR and BCR signaling to NF-κB by cleaving MALT-1 ubiquitin chains and therefore contributes to balance TCR/BCR-induced IKK/NF-KB signaling. Activated A20 might play an important role in protecting neural cells against autoimmune mediated demyelination.