Glycomic analysis of antibody indicates distinctive glycosylation profile in patients with autoimmune cholangitis.

Autor: Zhou X; Division of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, CA, 95616, USA; Department of Hepatobiliary Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. Electronic address: xzhou2009@hust.edu.cn., Kailemia MJ; Department of Chemistry, University of California, Davis, CA, 95616, USA. Electronic address: jkmuchena@yahoo.com., Sun Y; The Fifth Medical Center of PLA General Hospital, Beijing, 100039, China. Electronic address: sunying_302@yahoo.com., Shuai Z; Department of Rheumatology and Immunology, The First Affiliated Hospital of Anhui Medical University, Hefei, 230022, China. Electronic address: amushuaizw@163.com., Yang GX; Division of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, CA, 95616, USA. Electronic address: ygx1965@gmail.com., Dhaliwal S; Division of Gastroenterology and Hepatology, University of California, Davis, CA, USA. Electronic address: sandhaliwal@ucdavis.edu., Cristoferi L; Division of Gastroenterology and Center for Autoimmune Liver Diseases, Department of Medicine and Surgery, University of Milan-Bicocca, Monza, Italy. Electronic address: l.cristoferi@campus.unimib.it., Leung PSC; Division of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, CA, 95616, USA. Electronic address: psleung@ucdavis.edu., Invernizzi P; Division of Gastroenterology and Center for Autoimmune Liver Diseases, Department of Medicine and Surgery, University of Milan-Bicocca, Monza, Italy. Electronic address: pietro.invernizzi@unimib.it., Bowlus CL; Division of Gastroenterology and Hepatology, University of California, Davis, CA, USA. Electronic address: clbowlus@ucdavis.edu., Lebrilla CB; Department of Chemistry, University of California, Davis, CA, 95616, USA. Electronic address: cblebrilla@ucdavis.edu., Ansari AA; Division of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, CA, 95616, USA. Electronic address: pathaaa@emory.edu., Ridgway WM; Division of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, CA, 95616, USA. Electronic address: wmridgway@ucdavis.edu., Zhang W; Division of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, CA, 95616, USA. Electronic address: ddzhang@ucdavis.edu., Gershwin ME; Division of Rheumatology, Allergy and Clinical Immunology, University of California, Davis, CA, 95616, USA. Electronic address: megershwin@ucdavis.edu.
Jazyk: angličtina
Zdroj: Journal of autoimmunity [J Autoimmun] 2020 Sep; Vol. 113, pp. 102503. Date of Electronic Publication: 2020 Jun 13.
DOI: 10.1016/j.jaut.2020.102503
Abstrakt: Glycosylation of antibodies, particularly in the Fc domain, critically modulate the ability of antibodies to bind to FcRs, maintaining immune quiescence to achieve a finely orchestrated immune response. The removal of sialic acid and galactose residues dramatically alters the physiological function of IgGs, and alterations of Ig glycosylation have been associated with several autoimmune disorders. However, Ig glycosylation has not been extensively studied in autoimmune cholangitis. We applied triple quadruple mass spectroscopy with subsequent multiple reaction monitoring to elucidate the profile, composition and linkage of sugar residues of antibody glycans in patients with primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC) and healthy controls (HC). Agalactosylated, HexNAc terminated IgG1 glycoforms were enriched in both PBC and PSC. Levels of IgM glycans at site N439 and fucosylated glycans in J chain, were significantly decreased in PBC compared to PSC and HC. PSC patients had decreased bisecting glycoforms and increased biantennary glycoforms on IgA compared to PBC. Importantly, our data demonstrate the association of distinct branching and composition patterns of Ig glycoforms with disease severity and liver cirrhosis, which highlight the importance of glycan biology as a potential mechanism and/or a disease specific signal of inflammation.
(Copyright © 2020 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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