Figure 2.

Schematic Overview of potential pathophysiology of MS and role of ILCs. T-cells and B-cells infiltrate the CNS through a leaky blood-brain barrier whereby ILC subtypes that reside in the meninges release pro-inflammatory cytokines that influence the extent of CD4⁺ T-cell infiltration into the CNS. T-cells interact with B-cells and release cytokines and antibodies that cause inflammation which damages the myelin sheath of neurons and thereby induce demyelination. NK cells can also kill oligodendrocytes directly thereby potentially contributing to the extent of demyelination of the neurons. ILC2s are assumed to play a role in demyelination. LTis are assumed to play a role in the development of ELFs.