Abstract
Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is a kind of inflammatory neuropathy that has a gradual start and symmetrical sensory involvement. However, there are several clinical variances, suggesting that CIDP may represent a spectrum of linked disorders rather than a single disease entity. While the prevailing idea of CIDP pathogenesis is that cell-mediated and humoral processes interact in an abnormal immune response to damage peripheral neurons, the proportional roles of T cell and autoantibody responses are yet unknown. T cell responses to specified myelin antigens are responsible in animal models of spontaneous inflammatory neuropathy. Antibodies to Schwann cell, compact myelin, and nodal antigens have been found in different human inflammatory neuropathies. The roles of the cellular and humoral immune systems in the development of CIDP are discussed in this review. It is believed that, in the future, the identification of clinical phenotypes and the underlying disease processes would aid in the development of diagnostic and therapy options for CIDP.
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