한빛사 논문
Dávid Szamosvári,†,a Munhyung Bae,†,a,b Sunghee Bang,†,a Betsabeh Khoramian Tusi,‡,§,^ Chelsi D. Cassilly,† Sung-Moo Park,‡,§,^ Daniel B. Graham,‡,§,^ Ramnik J. Xavier,‡,§,^ Jon Clardy†,*
†Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School and Blavatnik Institute, Boston, MA 02115, USA ‡Broad Institute of MIT and Harvard, Cambridge, MA 02142 §Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114 ^Center for the Study of Inflammatory Bowel Disease, Massachusetts General Hospital, Boston, MA 02114
*Correspondence should be addressed to J. C.
aThese authors contributed equally to this work.
bPresent address: College of Pharmacy, Gachon University, Incheon 21936, Republic of Korea
Abstract
The human immune system detects potentially pathogenic microbes with receptors that respond to microbial metabolites. While the overall immune signaling pathway is known in considerable detail, the initial molecular signals, the microbially produced immunogens, for important diseases like Lyme disease (LD) are often not well-defined. The immunogens for LD are produced by the spirochete Borrelia burgdorferi, and a galactoglycerolipid (1) has been identified as a key trigger for the inflammatory immune response that characterizes LD. This report corrects the original structural assignment of 1 to 3, a change of an α-galactopyranose to an α-galactofuranose headgroup. The seemingly small change has important implications for the diagnosis, prevention, and treatment of LD.
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