期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 107, 期 4, 页码 1535-1540出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0909479107
关键词
microbial glycolipids; immune evasion; lyme disease
资金
- National Institute of Health [AI 074952, AI 45053, 69296]
- Foundation for Research Science and Technology [C08X0808]
- Cancer Research Institute
- Irvington Institute Fellowship Program of the Cancer Research Institute
- New Zealand Ministry of Business, Innovation & Employment (MBIE) [C08X0808] Funding Source: New Zealand Ministry of Business, Innovation & Employment (MBIE)
Invariant natural killer T cells (iNKT cells) respond to CD1d-presented glycolipids from Borrelia burgdorferi, the causative agent of Lyme disease. Although mouse and human iNKT cells respond to different antigens based on subtle differences in their fatty acids, the mechanism by which fatty acid structuredeterminesantigenicpotency is not well understood. Here we show that the mouse and human CD1d present glycolipids having different fatty acids, based in part upon a difference at a single amino acid position that is involved in positioning the sugar epitope. CD1d also can bind nonantigenic lipids, however, but unexpectedly, mouse CD1d orients the two aliphatic chains of a nonantigenic lipid rotated 180 degrees, causing a dramatic repositioning of the exposed sugar. Therefore, our data reveal the biochemical basis for the high degree of antigenic specificity of iNKT cells for certain fatty acids, and they suggest how microbes could alter fatty acid biosynthesis as an immune evasion mechanism.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据