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    Keywords: proliferation ; SYSTEM ; DISEASE ; PROTEIN ; MICE ; PATIENT ; MARKER ; ANTIGEN ; ANTIGENS ; T cell ; T cells ; T-CELL ; T-CELLS ; culture ; antibodies ; antibody ; MOUSE ; NERVOUS-SYSTEM ; LESIONS ; NUMBER ; COMPONENT ; DAMAGE ; cytoskeleton ; NETHERLANDS ; CD8(+) ; CENTRAL-NERVOUS-SYSTEM ; pathology ; AMYOTROPHIC-LATERAL-SCLEROSIS ; MULTIPLE-SCLEROSIS ; INTERFERON-GAMMA ; inflammation ; CD4(+) T-CELLS ; AUTOIMMUNE ENCEPHALOMYELITIS ; SERUM ; AUTOIMMUNITY ; IMMUNIZATION ; CYTOKINE ; RECOMBINANT ; RE ; SERUM ANTIBODIES ; LEVEL ; multiple sclerosis ; USA ; animal model ; central nervous system ; DEGENERATION ; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS ; correlates ; SENSORY NEURONOPATHY ; axonal damage ; MS LESIONS ; neurofilament light ; PROGRESSIVE MULTIPLE-SCLEROSIS ; spastic paresis
    Abstract: Axonal damage is the major cause of irreversible neurologic disability in patients with multiple sclerosis. Although axonal damage correlates with antibodies against neurotilament light (NF-L) protein, a major component of the axonal cytoskeleton, the possible pathogenic role of autoirnmunity to axonal antigens such as NF-L has so far been ignored. Here we show that Biozzi ABH mice immunized with NF-L protein develop neurologic disease characterized by spastic paresis and paralysis concomitant with axonal degeneration and inflammation primarily in the dorsal column of the spinal cord. The inflammatory central nervous system lesions were dominated by F4/80' macrophages/microglia and relatively low numbers of CD4(+) and CD8(+) T-cells. In splenocyte cultures, proliferation to NF-L was observed in CD4(+) T-cells accompanied by the production of the proinflammatory cytokine interferon-gamma. Elevated levels of circulating antibodies recognizing recombinant mouse NF-L were present in the serum, and immunoglobulin deposits were observed within axons in spinal cord lesions of mice exhibiting clinical disease. These data provide evidence that autoimmunity to NF-L protein induces axonal degeneration and clinical neurologic disease in mice, indicating that autoimmunity to axonal antigens, as described in multiple sclerosis, may be pathogenic rather than acting merely as a surrogate marker for axonal degeneration
    Type of Publication: Journal article published
    PubMed ID: 17413320
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