We identified two novel HLA alleles by NGS, HLA-B*51:395 and HLA-DQB1*06:478.
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Tissue degrading and remodelling molecules in giant cell arteritis.
Rheumatology (Oxford)
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Objectives: GCA is a granulomatous vasculitis affecting large vessels, leading to intimal occlusion accompanied by the accumulation of myofibroblasts. Histopathologically, GCA is characterized by destruction of the tunica media and hypertrophy of the intima with invasion of activated CD4+ T cells, macrophages and multinucleated giant cells (MNGCs). Despite these well-defined histopathological features, the molecular pathology of GCA has largely remained elusive.
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NPJ Syst Biol Appl
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T cells mediate pathogenesis of several autoimmune disorders by recognizing self-epitopes presented on Major Histocompatibility Complex (MHC) or Human Leukocyte Antigen (HLA) complex. The majority of autoantigens presented to T cells in various autoimmune disorders are not known, which has impeded autoantigen identification. Recent advances in immunopeptidomics have started to unravel the repertoire of antigenic epitopes presented on MHC.
View Article and Find Full Text PDFDynamic allostery in the peptide/MHC complex enables TCR neoantigen selectivity.
Nat Commun
January 2025
Department of Chemistry and Biochemistry, University of Notre Dame, Notre Dame, IN, USA.
The inherent antigen cross-reactivity of the T cell receptor (TCR) is balanced by high specificity. Surprisingly, TCR specificity often manifests in ways not easily interpreted from static structures. Here we show that TCR discrimination between an HLA-A*03:01 (HLA-A3)-restricted public neoantigen and its wild-type (WT) counterpart emerges from distinct motions within the HLA-A3 peptide binding groove that vary with the identity of the peptide's first primary anchor.
View Article and Find Full Text PDFSilica-mediated exacerbation of inflammatory arthritis: A novel murine model.
bioRxiv
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Objective: The mucosal origin hypothesis in rheumatoid arthritis (RA) posits that inhalant exposures, such as cigarette smoke and crystalline silica (c-silica), trigger immune responses contributing to disease onset. Despite the established risk posed by these exposures, the mechanistic link between inhalants, lung inflammation, and inflammatory arthritis remains poorly understood, partly from the lack of a suitable experimental model. As c-silica accelerates autoimmune phenotypes in lupus models and is a recognized risk factor for several autoimmune diseases, we investigated whether c-silica exposure could induce RA-like inflammatory arthritis in mice.
View Article and Find Full Text PDFA review on disease modifying pharmacologic therapies for sickle cell disease.
Ann Hematol
January 2025
Department of Internal Medicine, Section of Hematology/Oncology, University of Missouri-Kansas City, Kansas City, MO, 64108, USA.
Sickle cell disease (SCD) is an inherited hematologic disease caused by sickle hemoglobin as the predominant RBC hemoglobin or by sickle hemoglobin in combination with other abnormal β-hemoglobin variants like HbC, HbD and others. Sickling of erythrocytes under deoxygenated conditions is the basis of inflammatory and thrombotic cascades which result in multiple serious complications, leading to early morbidity and mortality. While HLA-matched allogeneic bone marrow transplantation is potentially curative, it has considerable limitations due to potential severe toxicities.
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