Glatiramer acetate Copaxone regulates nitric oxide and related cytokine secretion in experimental autoimmune encephalomyelitis
Yükleniyor...
Dosyalar
Tarih
2003
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Immunology Letters
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Nitric oxide (NO) is an important mediator involved in the pathogenesis of experimental autoimmune encephalomyelitis (EAE)
and multiple sclerosis (MS). We examined the effect of glatiramer acetate (GA), an agent with suppressing effect on EAE and of
therapeutic value for the treatment of MS, on the secretion of NO, as well as of the NO regulating cytokines. We observed that
induction of EAE leads to 4-fold elevation in NO secretion and that treatment of the EAE mice by GA indeed leads to a significant
reduction in the NO secretion by the splenocytes in response to the encephalitogen. A parallel decrease was observed in the secretion
of the NO inducing cytokine IL-1b. On the other hand, the secretion level of NO modulating cytokines IL-10 and IL-13 was
significantly augmented. The correlation between these findings and the therapeutic effect of GA is discussed.
Açıklama
Anahtar Kelimeler
Experimental autoimmune encephalomyelitis (EAE), Nitric oxide (NO), Th2 cytokines, Copaxone, Glatiramer acetate (GA)
Kaynak
Immunology Letters
WoS Q Değeri
Scopus Q Değeri
Cilt
Sayı
Künye
Kayhan, B. Aharoni, R. Arnon, R. (2003). Glatiramer acetate Copaxone regulates nitric oxide and related cytokine secretion in experimental autoimmune encephalomyelitis. Immunology Letters
