Increasing evidences show a global immune disregulation in multiple sclerosis (MS). The possible involvement of myelin and non-myelin (auto-)antigens in the autoaggressive process as well as the disregulation of both adaptive and innate immunity challenge the concept of specific immunotherapy. T cells at the boundary between innate and adaptive immunity, whose immunoregulatory role is becoming increasingly clear, have recently been shown to bear relevance for MS pathogenesis. Global immune interventions (and type I interferons may be considered as such) aimed at interfering with both innate and acquired immune responses seem to be a most promising therapeutic option in MS.
Global immune disregulation in multiple sclerosis: from the adaptive response to the innate immunity / Ristori, Giovanni; Montesperelli, C.; Perna, A.; Cannoni, S.; Battistini, L.; Borsellino, G.; Riccio, P.; Pesole, G.; Chersi, A.; Pozzilli, Carlo; Buttinelli, Carla; Salvetti, Marco. - In: JOURNAL OF NEUROIMMUNOLOGY. - ISSN 0165-5728. - 107(2):(2000), pp. 216-219. [10.1016/S0165-5728(00)00219-8]
Global immune disregulation in multiple sclerosis: from the adaptive response to the innate immunity
RISTORI, GIOVANNI;POZZILLI, Carlo;BUTTINELLI, Carla;SALVETTI, Marco
2000
Abstract
Increasing evidences show a global immune disregulation in multiple sclerosis (MS). The possible involvement of myelin and non-myelin (auto-)antigens in the autoaggressive process as well as the disregulation of both adaptive and innate immunity challenge the concept of specific immunotherapy. T cells at the boundary between innate and adaptive immunity, whose immunoregulatory role is becoming increasingly clear, have recently been shown to bear relevance for MS pathogenesis. Global immune interventions (and type I interferons may be considered as such) aimed at interfering with both innate and acquired immune responses seem to be a most promising therapeutic option in MS.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.