Regulation of experimental autoimmune encephalomyelitis by natural killer (NK) cells
B Zhang, T Yamamura, T Kondo, M Fujiwara… - The Journal of …, 1997 - rupress.org
B Zhang, T Yamamura, T Kondo, M Fujiwara, T Tabira
The Journal of experimental medicine, 1997•rupress.orgIn this report, we establish a regulatory role of natural killer (NK) cells in experimental
autoimmune encephalomyelitis (EAE), a prototype T helper cell type 1 (Th1)-mediated
disease. Active sensitization of C57BL/6 (B6) mice with the myelin oligodendrocyte
glycoprotein (MOG) 35-55 peptide induces a mild form of monophasic EAE. When mice
were deprived of NK cells by antibody treatment before immunization, they developed a
more serious form of EAE associated with relapse. Aggravation of EAE by NK cell deletion …
autoimmune encephalomyelitis (EAE), a prototype T helper cell type 1 (Th1)-mediated
disease. Active sensitization of C57BL/6 (B6) mice with the myelin oligodendrocyte
glycoprotein (MOG) 35-55 peptide induces a mild form of monophasic EAE. When mice
were deprived of NK cells by antibody treatment before immunization, they developed a
more serious form of EAE associated with relapse. Aggravation of EAE by NK cell deletion …
In this report, we establish a regulatory role of natural killer (NK) cells in experimental autoimmune encephalomyelitis (EAE), a prototype T helper cell type 1 (Th1)-mediated disease. Active sensitization of C57BL/6 (B6) mice with the myelin oligodendrocyte glycoprotein (MOG)35-55 peptide induces a mild form of monophasic EAE. When mice were deprived of NK cells by antibody treatment before immunization, they developed a more serious form of EAE associated with relapse. Aggravation of EAE by NK cell deletion was also seen in β2-microglobulin−/− (β2m−/−) mice, indicating that NK cells can play a regulatory role in a manner independent of CD8+ T cells or NK1.1+ T cells (NK–T cells). The disease enhancement was associated with augmentation of T cell proliferation and production of Th1 cytokines in response to MOG35-55. EAE passively induced by the MOG35-55-specific T cell line was also enhanced by NK cell deletion in B6, β2m−/−, and recombination activation gene 2 (RAG-2)−/− mice, indicating that the regulation by NK cells can be independent of T, B, or NK–T cells. We further showed that NK cells inhibit T cell proliferation triggered by antigen or cytokine stimulation. Taken together, we conclude that NK cells are an important regulator for EAE in both induction and effector phases.
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