Fernandez-Martin Amelia, Gonzalez-Rey Elena, Chorny Alejo, Ganea Doina, Delgado Mario
Institute of Parasitology and Biomedicine, CSIC, Granada 18100, Spain.
Eur J Immunol. 2006 Feb;36(2):318-26. doi: 10.1002/eji.200535430.
CD4(+)CD25(+) regulatory T cells (Treg) control the immune response to a variety of antigens, including self-antigens. Several models support the idea of the peripheral generation of CD4(+)CD25(+) Treg from CD4(+)CD25(-) T cells. Little is known about the endogenous factors and mechanisms controlling the peripheral expansion of CD4(+)CD25(+) Treg. In this study we report on the capacity of the vasoactive intestinal peptide (VIP), an immunosuppressive neuropeptide, to induce functional Treg in vivo during the development of experimental autoimmune encephalomyelitis (EAE), a multiple sclerosis model. The administration of VIP to EAE mice results in the expansion of the CD4(+)CD25(+), Foxp3-expressing T cells in the periphery and the nervous system, which inhibit encephalitogenic T cell activation. In addition to the increase in the number of CD4(+)CD25(+) Treg, VIP induces more efficient suppressors on a per cell basis. The VIP-generated CD4(+)CD25(+) Treg transfer suppression and significantly ameliorate the progression of the disease.
CD4(+)CD25(+)调节性T细胞（Treg）控制对多种抗原（包括自身抗原）的免疫反应。几种模型支持从CD4(+)CD25(-)T细胞外周生成CD4(+)CD25(+)Treg的观点。关于控制CD4(+)CD25(+)Treg外周扩增的内源性因素和机制知之甚少。在本研究中，我们报告了血管活性肠肽（VIP）（一种免疫抑制性神经肽）在实验性自身免疫性脑脊髓炎（EAE，一种多发性硬化模型）发展过程中在体内诱导功能性Treg的能力。给EAE小鼠施用VIP会导致外周和神经系统中表达Foxp3的CD4(+)CD25(+)T细胞扩增，从而抑制致脑炎T细胞的激活。除了CD4(+)CD25(+)Treg数量增加外，VIP在每个细胞基础上诱导更有效的抑制细胞。VIP产生的CD4(+)CD25(+)Treg转移抑制并显著改善疾病进展。
