Extracellular matrix protein N-glycosylation mediates immune self-tolerance in Drosophila melanogaster .

Autor:	Mortimer NT; School of Biological Sciences, Illinois State University, Normal, IL 61790; ntmorti@ilstu.edu., Fischer ML; School of Biological Sciences, Illinois State University, Normal, IL 61790., Waring AL; School of Biological Sciences, Illinois State University, Normal, IL 61790., Kr P; School of Biological Sciences, Illinois State University, Normal, IL 61790., Kacsoh BZ; Epigenetics Institute, Department of Cell and Developmental Biology, University of Pennsylvania, Philadelphia, PA 19104., Brantley SE; Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305., Keebaugh ES; Department of Biology, Emory University, Atlanta, GA 30322., Hill J; School of Biological Sciences, Illinois State University, Normal, IL 61790., Lark C; School of Biological Sciences, Illinois State University, Normal, IL 61790., Martin J; School of Biological Sciences, Illinois State University, Normal, IL 61790., Bains P; School of Biological Sciences, Illinois State University, Normal, IL 61790., Lee J; School of Biological Sciences, Illinois State University, Normal, IL 61790., Vrailas-Mortimer AD; School of Biological Sciences, Illinois State University, Normal, IL 61790., Schlenke TA; Department of Entomology, University of Arizona, Tucson, AZ 85719.
Jazyk:	angličtina
Zdroj:	Proceedings of the National Academy of Sciences of the United States of America [Proc Natl Acad Sci U S A] 2021 Sep 28; Vol. 118 (39).
DOI:	10.1073/pnas.2017460118
Abstrakt:	In order to respond to infection, hosts must distinguish pathogens from their own tissues. This allows for the precise targeting of immune responses against pathogens and also ensures self-tolerance, the ability of the host to protect self tissues from immune damage. One way to maintain self-tolerance is to evolve a self signal and suppress any immune response directed at tissues that carry this signal. Here, we characterize the Drosophila tuSz 1 mutant strain, which mounts an aberrant immune response against its own fat body. We demonstrate that this autoimmunity is the result of two mutations: 1) a mutation in the GCS1 gene that disrupts N-glycosylation of extracellular matrix proteins covering the fat body, and 2) a mutation in the Drosophila Janus Kinase ortholog that causes precocious activation of hemocytes. Our data indicate that N-glycans attached to extracellular matrix proteins serve as a self signal and that activated hemocytes attack tissues lacking this signal. The simplicity of this invertebrate self-recognition system and the ubiquity of its constituent parts suggests it may have functional homologs across animals. Competing Interests: The authors declare no competing interest. (Copyright © 2021 the Author(s). Published by PNAS.)
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu