摘要 : Multiple sclerosis is a disease characterized by inflammation and demyelination located in the central nervous system. Experimental autoimmune encephalomyelitis (EAE) is the most common animal model for multiple sclerosis (MS). Al... 展开 Multiple sclerosis is a disease characterized by inflammation and demyelination located in the central nervous system. Experimental autoimmune encephalomyelitis (EAE) is the most common animal model for multiple sclerosis (MS). Although the roles of T cells in MS/EAE have been well investigated, little is known about the functions of other immune cells in the neuroinflammation model. Here we found that an essential cytokine transforming growth factor beta (TGF-beta) which could mediate the differentiation of Th17/regulatory T cells was implicated in the natural killer (NK) cells' activity in EAE. In EAE mice, TGF-beta expression was first increased at the onset and then decreased at the peak, but the expressions of TGF-beta receptors and downstream molecules were not affected in EAE. When we immunized the mice with MOG antigen, it was revealed that TGF-beta treatment reduced susceptibility to EAE with a lower clinical score than the control mice without TGF-beta. Consistently, inflammatory cytokine production was reduced in the TGF-beta treated group, especially with downregulated pathogenic interleukin-17 in the central nervous system tissue. Furthermore, TGF-beta could increase the transcription level of NK cell marker NCR1 both in the spleen and in the CNS without changing other T cell markers. Meanwhile TGF-beta promoted the proliferation of NK cell proliferation. Taken together, our data demonstrated that TGF-beta could confer protection against EAE model in mice through NK cells, which would be useful for the clinical therapy of MS. 收起