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Mol Neurodegener ; 13(1): 42, 2018 08 09.
Article in English | MEDLINE | ID: mdl-30092791

ABSTRACT

BACKGROUND: The major histocompatibility complex I (MHCI) is a key molecule for the interaction of mononucleated cells with CD8+T lymphocytes. We previously showed that MHCI is upregulated in the spinal cord microglia and motor axons of transgenic SOD1G93A mice. METHODS: To assess the role of MHCI in the disease, we examined transgenic SOD1G93A mice crossbred with ß2 microglobulin-deficient mice, which express little if any MHCI on the cell surface and are defective for CD8+ T cells. RESULTS: The lack of MHCI and CD8+ T cells in the sciatic nerve affects the motor axon stability, anticipating the muscle atrophy and the disease onset. In contrast, MHCI depletion in resident microglia and the lack of CD8+ T cell infiltration in the spinal cord protect the cervical motor neurons delaying the paralysis of forelimbs and prolonging the survival of SOD1G93A mice. CONCLUSIONS: We provided straightforward evidence for a dual role of MHCI in the peripheral nervous system (PNS) compared to the CNS, pointing out regional and temporal differences in the clinical responses of ALS mice. These findings offer a possible explanation for the failure of systemic immunomodulatory treatments and suggest new potential strategies to prevent the progression of ALS.


Subject(s)
Amyotrophic Lateral Sclerosis/immunology , CD8-Positive T-Lymphocytes/immunology , Histocompatibility Antigens Class I/immunology , Peripheral Nervous System/immunology , Spinal Cord/immunology , Amyotrophic Lateral Sclerosis/pathology , Animals , CD8-Positive T-Lymphocytes/pathology , Disease Models, Animal , Disease Progression , Mice , Mice, Inbred C57BL , Mice, Transgenic , Peripheral Nervous System/pathology , Spinal Cord/pathology
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