neuritogenic

This can be demonstrated in NOD mice in which a point mutation in the autoimmune regulator (Aire) gene results in the reduced expression of P0 in the thymus and a concomitant increase of P0 specific T cells in the periphery. 107 Similarly, autoimmunity is shifted towards the peripheral nerve in another NOD model deficient for isoforms of ICAM-1. 108 Altered expression of ICAM-1 on thymic epithelial cells transforms selection of T cells from a diabetogenic into a neuritogenic repertoire. 108 Studies such as these highlight the critical role of regulatory mechanisms in maintaining immune homeostasis and the impact that changes to regulation can have on the development of disease.

2015 February 12, Emily K Mathey et al., “Chronic inflammatory demyelinating polyradiculoneuropathy: from pathology to phenotype”, in Journal of Neurology, Neurosurgery, and Psychiatry, volume 86, →DOI