EXPRESSION OF INTEGRINS IN EXPERIMENTAL AUTOIMMUNE NEURITIS AND GUILLAIN-BARRE-SYNDROME

Integrins are a subclass of adhesion molecules that mediate cell-cell and cell-extracellular matrix interactions. Integrins influence transe ndothelial migration of lymphocytes and monocytes and are suitable tar gets for experimental immunotherapy. They are critically involved in t he pathogenesis of autoimmune neuritis and abnormally expressed in hum an neuropathies. Also, the role of integrins in myelination, neurite o utgrowth, and nerve regeneration suggests that they could be involved in the recovery phase of immune-mediated neuropathies. We investigated by immunohistochemistry the expression of a number of integrin subuni ts during the course of experimental autoimmune neuritis (EAN). Result s were compared with the human immune neuropathy Guillain-Barre: syndr ome (GBS) and extended in vitro. Inflammation and demyelination in bot h EAN and GBS induced the down-regulation of beta 4 integrin in Schwan n cells (SCs), whereas loss of alpha 2 was noted only in EAN. When axo nal loss was present, SCs displayed alpha 5 integrin, in both EAN and GBS. In vitro, basal lamina and inflammatory cytokines modulated the e xpression of beta 4 in SCs, but they did not influence alpha 2 and alp ha 5 expression. Finally, integrins were differentially expressed in b lood vessels during EAN. In conclusion, the spatiotemporal changes in integrin expression may be used to characterize, stage, and better und erstand the pathogenesis and evolution of inflammation during GBS and EAN. This may help to establish useful, novel therapy for immune-media ted neuropathies.