CD26/DPIV in Diseases of the Central Nervous System
The current model for the initiation of T cell-mediated autoimmune inflammatory disease of the central nervous system (CNS) includes peripheral activation of T cells specific for myelin antigens and T helper cell type 1 (Thl) differentiation (Martin et al 1992; Miller and Shevach, 1998). Naive CD4+ T cells develop into either of two major subsets of Th cells that produce distinct sets of cytokines (O’Garra et al 1997). It is widely accepted that Thl cells, critical for cell-mediated immunity by their production of interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α) and lymphotoxin are involved in the immunopathology of organ-specific autoimmune disease (O’Garra et al 1997), including diseases of the CNS (Martin et al 1992). A role as regulators has been suggested for Th2 cells (O’Garra et al 1997) and cells producing transforming growth factor-ß (TGF-ß), recently characterized as Th3 and Tr (regulatory) CD4+ T cells (Weiner 1997). Once primed, autoreactive T cells are able to cross the blood-brain barrier and respond to CNS antigens in situ. Leukocyte accumulation and lesion formation in inflammatory CNS disorders critically depend on antigendriven Thl T cell restimulation in the CNS compartment (Karpus and Ransohoff 1998; Karpus 1999).
KeywordsHydrolysis Prostaglandin Neurol Methylprednisolone Encephalomyelitis
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