Guilliams Martin, Oldenhove Guillaume, Noel Wim, Hérin Michel, Brys Lea, Loi Patrizia, Flamand Véronique, Moser Muriel, De Baetselier Patrick, Beschin Alain
Department of Molecular and Cellular Interactions, Vlaams Instituut voor Biotechnologie, Vrije Universiteit Brussel, 1050 Brussels, Belgium.
J Immunol. 2007 Sep 1;179(5):2748-57. doi: 10.4049/jimmunol.179.5.2748.
Tolerance to African trypanosomes requires the production of IFN-gamma in the early stage of infection that triggers the development of classically activated macrophages controlling parasite growth. However, once the first peak of parasitemia has been controlled, down-regulation of the type 1 immune response has been described. In this study, we have evaluated whether regulatory T cells (Tregs) contribute to the limitation of the immune response occurring during Trypanosoma congolense infection and hereby influence the outcome of the disease in trypanotolerant C57BL/6 host. Our data show that Foxp3+ Tregs originating from the naturally occurring Treg pool expanded in the spleen and the liver of infected mice. These cells produced IL-10 and limited the production of IFN-gamma by CD4+ and CD8+ effector T cells. Tregs also down-regulated classical activation of macrophages resulting in reduced TNF-alpha production. The Treg-mediated suppression of the type 1 inflammatory immune response did not hamper parasite clearance, but was beneficial for the host survival by limiting the tissue damages, including liver injury. Collectively, these data suggest a cardinal role for naturally occurring Tregs in the development of a trypanotolerant phenotype during African trypanosomiasis.
对非洲锥虫的耐受性需要在感染早期产生干扰素-γ,这会触发经典活化巨噬细胞的发育,从而控制寄生虫的生长。然而,一旦寄生虫血症的第一个高峰得到控制,就会出现1型免疫反应的下调。在本研究中,我们评估了调节性T细胞(Tregs)是否有助于限制刚果锥虫感染期间发生的免疫反应,并由此影响锥虫耐受型C57BL/6宿主的疾病结局。我们的数据表明,源自天然Treg池的Foxp3+ Tregs在感染小鼠的脾脏和肝脏中扩增。这些细胞产生白细胞介素-10,并限制CD4+和CD8+效应T细胞产生干扰素-γ。Tregs还下调巨噬细胞的经典活化,导致肿瘤坏死因子-α的产生减少。Treg介导的对1型炎症免疫反应的抑制并未妨碍寄生虫的清除,但通过限制包括肝损伤在内的组织损伤,对宿主存活有益。总的来说,这些数据表明天然Tregs在非洲锥虫病期间锥虫耐受表型的发展中起关键作用。