translation agency

NLM AIDSLINE
Enhancement of Th2 response in IL-6-deficient mice immunized with myelin oligodendrocyte glycoprotein.
Okuda Y; Sakoda S; Saeki Y; Kishimoto T; Yanagihara T; Neuroimmunology
July 30, 2000
J Neuroimmunol. 2000 Jun 26;105(2):120-3. Unique Identifier : AIDSLINE

To investigate the mechanism for the resistance of IL-6-deficient mice to experimental autoimmune encephalomyelitis (EAE), we examined the production of cytokines in lymph nodes (LNs) of wild-type and IL-6-deficient mice immunized with myelin oligodendrocyte glycoprotein (MOG) by reverse transcriptase-polymerase chain reaction analysis. Significant up-regulation of IL-4 production and down-regulation of IFN-gamma production were found in LNs from IL-6-deficient mice as compared to LNs from wild-type mice. Administration of IL-6, which caused typical EAE in IL-6-deficient mice immunized with MOG, reduced IL-4 production but did not restore IFN-gamma production in LNs of IL-6-deficient mice. These results implied that the resistance of IL-6-deficient mice to EAE might be mainly due to enhancement of Th2 response.

JOURNAL ARTICLE Animal Encephalomyelitis, Experimental Autoimmune/PREVENTION & CONTROL Female Immunization Interferon Type II/BIOSYNTHESIS Interleukin-10/GENETICS Interleukin-4/GENETICS Interleukin-6/DEFICIENCY/*PHYSIOLOGY Mice Mice, Inbred C57BL Myelin-Associated Glycoprotein/*IMMUNOLOGY RNA, Messenger/ANALYSIS Support, Non-U.S. Gov't Th2 Cells/*IMMUNOLOGY

www.aegis.org