CD4 T cells mediate axonal damage and spinal cord motor neuron apoptosis in murine p0106-125-induced experimental autoimmune neuritis.

摘要: The pathogenesis of inflammatory autoimmune diseases the peripheral nervous system, leading to demyelination and/or axonal damage, remains incompletely understood. In particular, it is controversial regarding extent which (i) autoimmune-mediated destruction nerves results in secondary damage central and (ii) CD4 CD8 T cells contribute disease. To address these issues, we applied murine model P0106–125-induced experimental neuritis. Immunization C57BL/6 mice with P0106–125 resulted severe mild demyelination. Importantly, developed a “dying-back” axonopathy apoptosis large fraction neurons anterior horn lumbar thoracic spinal cord progressive neurogenic muscular atrophy. cell-depletion experiments identified CD4, but not CD8, as important mediators represented major cellular source antigen-specific interferon-γ interleukin-17 production, regulated number tumor necrosis factor-positive inducible nitric oxide synthase-positive macrophages diseased sciatic nerve, mediated subsequent neuronal contrast, was only slightly ameliorated cell-depleted mice. conclusion, neuritis cell-mediated disease that affects both systems.