ArticleImmunology2010
DM influences the abundance of major histocompatibility complex class II alleles with low affinity for class II-associated invariant chain peptides via multiple mechanisms.
Article in Immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- HLA associations in inflammatory arthritis: emerging mechanisms and clinical implications.Nature reviews. Rheumatology · 2019Review
- Epitope Selection for HLA-DQ2 Presentation: Implications for Celiac Disease and Viral Defense.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Human Intestinal Enteroids Model MHC-II in the Gut Epithelium.Frontiers in immunology · 2019Article
- Mechanisms underlying the lack of endogenous processing and CLIP-mediated binding of the invariant chain by HLA-DPScientific reports · 2018Article
- Human leukocyte Antigen-DM polymorphisms in autoimmune diseases.Open biology · 2016Review
- Exogenous antigens bind MHC class II first, and are processed by cathepsins later.Molecular immunology · 2015Review
- pH-susceptibility of HLA-DO tunes DO/DM ratios to regulate HLA-DM catalytic activity.Scientific reports · 2015Article
- The MHC class II cofactor HLA-DM interacts with Ig in B cells.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- An unstable Th epitope of P. falciparum fosters central memory T cells and anti-CS antibody responses.PloS one · 2014Article
- Exposing the Specific Roles of the Invariant Chain Isoforms in Shaping the MHC Class II Peptidome.Frontiers in immunology · 2013Review
- MHC Class II Protein Turnover In vivo and Its Relevance for Autoimmunity in Non-Obese Diabetic Mice.Frontiers in immunology · 2013Review
- Accelerated turnover of MHC class II molecules in nonobese diabetic mice is developmentally and environmentally regulated in vivo and dispensable for autoimmunity.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- HLA-DO acts as a substrate mimic to inhibit HLA-DM by a competitive mechanism.Nature structural & molecular biology · 2013Article
- Pulse-chase analysis for studies of MHC class II biosynthesis, maturation, and peptide loading.Methods in molecular biology (Clifton, N.J.) · 2013Article
- An insertion mutant in DQA1*0501 restores susceptibility to HLA-DM: implications for disease associations.Journal of immunology (Baltimore, Md. : 1950) · 2011Article
- I-Ag7 is subject to post-translational chaperoning by CLIP.International immunology · 2010Article
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
DM catalyses class II-associated invariant chain peptide (CLIP) release, edits the repertoire of peptides bound to major histocompatibility complex (MHC) class II molecules, affects class II structure, and thereby modulates binding of conformation-sensitive anti-class II antibodies. Here, we investigate the ability of DM to enhance the cell surface binding of monomorphic antibodies. We show that this enhancement reflects increases in cell surface class II expression and total cellular abundance, but notably these effects are selective for particular alleles. Evidence from analysis of cellular class II levels after cycloheximide treatment and from pulse-chase experiments indicates that DM increases the half-life of affected alleles. Unexpectedly, the pulse-chase experiments also revealed an early effect of DM on assembly of these alleles. The allelically variant feature that correlates with susceptibility to these DM effects is low affinity for CLIP; DM-dependent changes in abundance are reduced by invariant chain (CLIP) mutants that enhance CLIP binding to class II. We found evidence that DM mediates rescue of peptide-receptive DR0404 molecules from inactive forms in vitro and evidence suggesting that a similar process occurs in cells. Thus, multiple mechanisms, operating along the biosynthetic pathway of class II molecules, contribute to DM-mediated increases in the abundance of low-CLIP-affinity alleles.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.