Communication between pathogenic T cells and myeloid cells in neuroinflammatory disease

Abstract

Clinical and experimental data suggest that T helper (T(H)) cells are involved in the pathogenicity of experimental autoimmune encephalomyelitis (EAE) and multiple sclerosis (MS), but it is unlikely that they are directly responsible for the observed demyelination and axonal loss. Instead, the cell population that targets the destruction of oligodendrocytes and axons, and the mechanism exploited by central nervous system (CNS)-invading encephalitogenic T(H) cells to instruct these cells to mediate tissue damage, are still under debate. Mature myeloid cells form a prominent component of the neuroinflammatory infiltrates and are the suspected culprits behind the CNS injury due to their arsenal of toxic factors. Here, we describe the process of encephalitogenic T(H) cell activation followed by their entry into the CNS and discuss how pathogenic T(H) cells influence the myeloid compartment.