最近被定性的“先天淋巴細(xì)胞”(ILCs) 在功能上可被劃分成三類,。第一類的ILCs 產(chǎn)生干擾素-γ,；第二類的ILCs 表達(dá)白介素-5,、白介素-13和雙調(diào)蛋白；第三類的ILCs 產(chǎn)生白介素-17A和白介素-22,。ILCs在適應(yīng)性免疫存在時(shí)的功能及它們影響適應(yīng)性免疫細(xì)胞反應(yīng)的潛力在很大程度上是不知道的?，F(xiàn)在用小鼠所做的一項(xiàng)研究顯示，第三類的ILCs處理和呈現(xiàn)抗原,，并通過一個(gè)依賴于“MHC-class-II”的機(jī)制控制CD4+ T-細(xì)胞對(duì)小腸共生菌的反應(yīng),。這一發(fā)現(xiàn)也許有助于了解與對(duì)共生菌的炎性宿主免疫反應(yīng)相關(guān)的人類慢性病的病理。(生物谷Bioon.com)
生物谷推薦英文摘要：
Nature doi: 10.1038/nature12240
Innate lymphoid cells regulate CD4+ T-cell responses to intestinal commensal bacteria
Matthew R. Hepworth,Laurel A. Monticelli, Thomas C. Fung,Carly G. K. Ziegler,Stephanie Grunberg,Rohini Sinha,Adriana R. Mantegazza,Hak-Ling Ma, Alison Crawford, Jill M. Angelosanto,E. John Wherry,Pandelakis A. Koni,Frederic D. Bushman,Charles O. Elson, Gérard Eberl,David Artis& Gregory F. Sonnenberg
Innate lymphoid cells (ILCs) are a recently characterized family of immune cells that have critical roles in cytokine-mediated regulation of intestinal epithelial cell barrier integrity. Alterations in ILC responses are associated with multiple chronic human diseases, including inflammatory bowel disease, implicating a role for ILCs in disease pathogenesis. Owing to an inability to target ILCs selectively, experimental studies assessing ILC function have predominantly used mice lacking adaptive immune cells. However, in lymphocyte-sufficient hosts ILCs are vastly outnumbered by CD4+ T cells, which express similar profiles of effector cytokines. Therefore, the function of ILCs in the presence of adaptive immunity and their potential to influence adaptive immune cell responses remain unknown. To test this, we used genetic or antibody-mediated depletion strategies to target murine ILCs in the presence of an adaptive immune system. We show that loss of retinoic-acid-receptor-related orphan receptor-γt-positive (RORγt+) ILCs was associated with dysregulated adaptive immune cell responses against commensal bacteria and low-grade systemic inflammation. Remarkably, ILC-mediated regulation of adaptive immune cells occurred independently of interleukin (IL)-17A, IL-22 or IL-23. Genome-wide transcriptional profiling and functional analyses revealed that RORγt+ ILCs express major histocompatibility complex class II (MHCII) and can process and present antigen. However, rather than inducing T-cell proliferation, ILCs acted to limit commensal bacteria-specific CD4+ T-cell responses. Consistent with this, selective deletion of MHCII in murine RORγt+ ILCs resulted in dysregulated commensal bacteria-dependent CD4+ T-cell responses that promoted spontaneous intestinal inflammation. These data identify that ILCs maintain intestinal homeostasis through MHCII-dependent interactions with CD4+ T cells that limit pathological adaptive immune cell responses to commensal bacteria.
