CD26/DPIV in Diseases of the Central Nervous System

摘要: The current model for the initiation of T cell-mediated autoimmune inflammatory disease central nervous system (CNS) includes peripheral activation cells specific myelin antigens and helper cell type 1 (Thl) differentiation (Martin et al 1992; Miller Shevach, 1998). Naive CD4+ develop into either two major subsets Th that produce distinct sets cytokines (O’Garra 1997). It is widely accepted Thl cells, critical immunity by their production interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α) lymphotoxin are involved in immunopathology organ-specific 1997), including diseases CNS 1992). A role as regulators has been suggested Th2 1997) producing transforming growth factor-s (TGF-s), recently characterized Th3 Tr (regulatory) (Weiner Once primed, autoreactive able to cross blood-brain barrier respond situ. Leukocyte accumulation lesion formation disorders critically depend on antigendriven restimulation compartment (Karpus Ransohoff 1998; Karpus 1999).