拓展抗原特异性调节网络以治疗自身免疫病。
Expanding antigen-specific regulatory networks to treat autoimmunity.
机构信息
Julia McFarlane Diabetes Research Centre (JMDRC), and Department of Microbiology, Immunology and Infectious Diseases, Snyder Institute for Chronic Diseases and Hotchkiss Brain Institute, Cumming School of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada.
Institut D'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, 08036, Spain.
出版信息
Nature. 2016 Feb 25;530(7591):434-40. doi: 10.1038/nature16962. Epub 2016 Feb 17.
Regulatory T cells hold promise as targets for therapeutic intervention in autoimmunity, but approaches capable of expanding antigen-specific regulatory T cells in vivo are currently not available. Here we show that systemic delivery of nanoparticles coated with autoimmune-disease-relevant peptides bound to major histocompatibility complex class II (pMHCII) molecules triggers the generation and expansion of antigen-specific regulatory CD4(+) T cell type 1 (TR1)-like cells in different mouse models, including mice humanized with lymphocytes from patients, leading to resolution of established autoimmune phenomena. Ten pMHCII-based nanomedicines show similar biological effects, regardless of genetic background, prevalence of the cognate T-cell population or MHC restriction. These nanomedicines promote the differentiation of disease-primed autoreactive T cells into TR1-like cells, which in turn suppress autoantigen-loaded antigen-presenting cells and drive the differentiation of cognate B cells into disease-suppressing regulatory B cells, without compromising systemic immunity. pMHCII-based nanomedicines thus represent a new class of drugs, potentially useful for treating a broad spectrum of autoimmune conditions in a disease-specific manner.
调节性 T 细胞有望成为自身免疫性疾病治疗干预的靶点,但目前尚无能够在体内扩增抗原特异性调节性 T 细胞的方法。在这里,我们展示了全身性递送至与自身免疫性疾病相关的肽与主要组织相容性复合体 II(pMHCII)分子结合的纳米粒子,可触发不同小鼠模型中抗原特异性调节性 CD4(+)T 细胞 1(TR1)样细胞的产生和扩增,包括用人患者淋巴细胞人源化的小鼠,从而解决已建立的自身免疫现象。十种基于 pMHCII 的纳米药物具有相似的生物学效应,而与遗传背景、同源 T 细胞群体的流行率或 MHC 限制无关。这些纳米药物促进疾病引发的自身反应性 T 细胞分化为 TR1 样细胞,进而抑制载有自身抗原的抗原呈递细胞,并驱动同源 B 细胞分化为抑制疾病的调节性 B 细胞,而不损害全身免疫。因此,基于 pMHCII 的纳米药物代表了一类新的药物,可能对以疾病特异性方式治疗广泛的自身免疫性疾病有用。