Genomic sequence of HLA-DQB1*03:01:01:60, -DQB1*03:01:01:61, -DQB1*03:01:01:62, -DQB1*03:01:01:63, -DQB1*03:02:01:23, -DQB1*03:02:01:24, -DQB1*03:02:01:25 and -DQB1*03:03:02:14 alleles in Spanish individuals.
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http://dx.doi.org/10.1111/tan.15634 | DOI Listing |
J Biol Chem
September 2024
Antiger Therapeutics Inc., St Louis, Missouri, USA. Electronic address:
HLA-DQ molecules drive unwanted alloimmune responses after solid-organ transplants and several autoimmune diseases, including type 1 diabetes and celiac disease. Biologics with HLA molecules as part of the design are emerging therapeutic options for these allo- and autoimmune conditions. However, the soluble α and β chains of class II HLA molecules do not dimerize efficiently without their transmembrane domains, which hinders their production.
View Article and Find Full Text PDFEBioMedicine
October 2023
Division of Rheumatology, Department of Medicine, Solna, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden; Center for Molecular Medicine, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden. Electronic address:
Background: In patients with idiopathic inflammatory myopathies (IIM), autoantibodies are associated with specific clinical phenotypes suggesting a pathogenic role of adaptive immunity. We explored if autoantibody profiles are associated with specific HLA genetic variants and clinical manifestations in IIM.
Methods: We included 1348 IIM patients and determined the occurrence of 14 myositis-specific or -associated autoantibodies.
J Allergy Clin Immunol
December 2021
Department of Medicine, University of Colorado, Aurora, Colo. Electronic address:
Background: Total serum IgE (tIgE) is an important intermediate phenotype of allergic disease. Whole genome genetic association studies across ancestries may identify important determinants of IgE.
Objective: We aimed to increase understanding of genetic variants affecting tIgE production across the ancestry and allergic disease spectrum by leveraging data from the National Heart, Lung and Blood Institute Trans-Omics for Precision Medicine program; the Consortium on Asthma among African-ancestry Populations in the Americas (CAAPA); and the Atopic Dermatitis Research Network (N = 21,901).
J Invest Dermatol
June 2018
Department of Dermatology and Allergology, University Hospital, Ludwig-Maximilian-University, Munich, Germany. Electronic address:
Generalized pustular psoriasis (GPP) is the most severe psoriasis variant. Mutations in the IL-36 antagonist IL36RN, in CARD14 or AP1S3 provide genetic evidence for autoinflammatory etiology but cannot explain its pathogenesis completely. Here we demonstrate that unopposed IL-36 signaling promotes antigen-driven and likely pathogenic T-helper type 17 (Th17) responses in GPP.
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