Early administration of IL-12 suppresses EAE through induction of interferon-gamma.
Recent findings have shown that IL-12, a key inducer of Th1 cell development, is not required in the pathogenesis of experimental autoimmune encephalomyelitis (EAE) as severe CNS inflammatory demyelination can develop in the absence of IL-12 or IL-12 responsiveness. These data raised the possibility of an immunomodulatory action of IL-12 in this disease model. We show here that IL-12 suppresses MOG35-55-induced EAE in the C57BL/6 mouse when administered during the early induction phase of the disease. The inhibitory effect is interferon-gamma-(IFN-gamma)-dependent, as clearly shown by lack of suppression in IFN-gamma-deficient mice, and is also accompanied by inhibition of mRNA expression of the proinflammatory cytokine IL-17.
Gran
Bruno
B
Department of Neurology, Thomas Jefferson University, 300 Hospital for Neuroscience, 900 Walnut Street, Philadelphia, PA 19107, USA. bruno.gran@jefferson.edu
Chu
Niansheng
N
Zhang
Guang-Xian
GX
Yu
Shuo
S
Li
Yonghai
Y
Chen
Xiao-Han
XH
Kamoun
Malek
M
Rostami
Abdolmohamad
A
D000818:Animals; D004334:Drug Administration Schedule; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology* / Q000378:metabolism / Q000517:prevention & control*; D007166:Immunosuppressive Agents / Q000008:administration & dosage*; D007371:Interferon-gamma / Q000096:biosynthesis* / Q000502:physiology; D018664:Interleukin-12 / Q000008:administration & dosage*; D051379:Mice; D008810:Mice, Inbred C57BL
D007166:Immunosuppressive Agents; D018664:Interleukin-12; D007371:Interferon-gamma