FOXP3型
免疫系统
免疫学
生物
周边公差
交感神经系统
实验性自身免疫性脑脊髓炎
抗原
转化生长因子β
免疫耐受
神经科学
转化生长因子
细胞生物学
内分泌学
血压
作者
Sourojit Bhowmick,Anurag Singh,Richard A. Flavell,Robert B. Clark,James O’Rourke,Robert E. Cone
摘要
Abstract The sympathetic nervous system can control the number of regulatory T cells by modulating the level of TGF-β in the periphery. CD4+FoxP3+ Tregs are essential mediators of the peripheral immune response to self-antigens. Accordingly, the homeostatic regulation of Treg activity and number would impact on the immune response to both self- and non-self antigens. Because the sympathetic nervous system (SNS) interacts chemically and physically with the central and peripheral immune system and exerts a direct influence on antigen-presenting cells and effector lymphocytes, we have investigated the effect of chemical ablation of the SNS on the number and function of peripheral Treg. Removal of murine peripheral sympathetic innervation by 6-hydroxydopamine induced an increase in splenic and lymph node CD4+FoxP3+ Tregs by a TGF-β-dependent mechanism. Further, this increase in Tregs coincides with an inhibition of the induction of experimental autoimmune encephalomyelitis. Our results demonstrate that the SNS is an important contributor to the maintenance of peripheral Treg and TGF-β acts as a bridge between the immune system and the nervous system. Neurological events mediated by the SNS, such as a stress response, may affect the number of T cells that regulate an immune response. Additionally, targeting Tregs via the SNS may be a novel approach to the prevention or treatment of autoimmune diseases.
科研通智能强力驱动
Strongly Powered by AbleSci AI