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Pathological mechanism of autoimmune encephalomyelitis regulated by vagus nerve innervation

 In general, various external stimuli associated with excess stress and chronic pain induce synaptic plasticity and dysfunction of both the central nervous system (CNS) and glial cells (astrocytes and microglia). Abnormality of the neural network and/or glial cells triggers various disease-based phenotypes, such as psychiatric disorders, persistent pain, dementia and immunodeficiency. On the other hand, it has been suggested that dysfunction of the CNS leads to peripheral symptoms through various efferent controls. However, the causal relationship between synaptic plasticity and peripheral phenomena, such as chronic pain and immunodeficiency, has not yet been clarified. To investigate these mechanisms, it is crucial that we understand “neuro-immunity” mediated by neural and glial functions. In this symposium, we will introduce the latest research on “neuro-immunity” derived from dysfunction of the CNS and glial cells, which is associated with various diseases. We hope that our discussions will provide the audience insights that could lead to the discovery of new treatments. 

Latest research on next-generation "neuro-immunology": multiangle approaches in the CNS and glia cells

The 141st Annual Meeting of the Pharmaceutical Society of Japan (Hiroshima)

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[GS03-1]Pathological mechanism of autoimmune encephalomyelitis regulated by vagus nerve innervation

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