Dissecting MHC class II export, B cell maturation, and DM stability defects in invariant chain mutant mice.

Invariant (Ii) chain loss causes defective class II export, B cell maturation, and reduced DM stability. In this study, we compare Ii chain and class II mutant mouse phenotypes to dissect these disturbances. The present results demonstrate that ER retention of alphabeta complexes, and not beta-chain...

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Main Authors: Koonce, C, Bikoff, E
Format: Journal article
Language:English
Published: 2004
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author Koonce, C
Bikoff, E
author_facet Koonce, C
Bikoff, E
author_sort Koonce, C
collection OXFORD
description Invariant (Ii) chain loss causes defective class II export, B cell maturation, and reduced DM stability. In this study, we compare Ii chain and class II mutant mouse phenotypes to dissect these disturbances. The present results demonstrate that ER retention of alphabeta complexes, and not beta-chain aggregates, disrupts B cell development. In contrast, we fail to detect class II aggregates in Ii chain mutant thymi. Ii chain loss in NOD mice leads to defective class II export and formation of alphabeta aggregates, but in this background, downstream signals are misregulated and mature B cells develop normally. Finally, Ii chain mutant strains all display reduced levels of DM, but mice expressing either p31 or p41 alone, and class II single chain mutants, are indistinguishable from wild type. We conclude that Ii chain contributions as a DM chaperone are independent of its role during class II export. This Ii chain/DM partnership favors class II peptide loading via conventional pathway(s).
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spelling oxford-uuid:0055d625-c077-42b9-a601-3cbf42dfb9282022-03-26T08:28:59ZDissecting MHC class II export, B cell maturation, and DM stability defects in invariant chain mutant mice.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:0055d625-c077-42b9-a601-3cbf42dfb928EnglishSymplectic Elements at Oxford2004Koonce, CBikoff, EInvariant (Ii) chain loss causes defective class II export, B cell maturation, and reduced DM stability. In this study, we compare Ii chain and class II mutant mouse phenotypes to dissect these disturbances. The present results demonstrate that ER retention of alphabeta complexes, and not beta-chain aggregates, disrupts B cell development. In contrast, we fail to detect class II aggregates in Ii chain mutant thymi. Ii chain loss in NOD mice leads to defective class II export and formation of alphabeta aggregates, but in this background, downstream signals are misregulated and mature B cells develop normally. Finally, Ii chain mutant strains all display reduced levels of DM, but mice expressing either p31 or p41 alone, and class II single chain mutants, are indistinguishable from wild type. We conclude that Ii chain contributions as a DM chaperone are independent of its role during class II export. This Ii chain/DM partnership favors class II peptide loading via conventional pathway(s).
spellingShingle Koonce, C
Bikoff, E
Dissecting MHC class II export, B cell maturation, and DM stability defects in invariant chain mutant mice.
title Dissecting MHC class II export, B cell maturation, and DM stability defects in invariant chain mutant mice.
title_full Dissecting MHC class II export, B cell maturation, and DM stability defects in invariant chain mutant mice.
title_fullStr Dissecting MHC class II export, B cell maturation, and DM stability defects in invariant chain mutant mice.
title_full_unstemmed Dissecting MHC class II export, B cell maturation, and DM stability defects in invariant chain mutant mice.
title_short Dissecting MHC class II export, B cell maturation, and DM stability defects in invariant chain mutant mice.
title_sort dissecting mhc class ii export b cell maturation and dm stability defects in invariant chain mutant mice
work_keys_str_mv AT kooncec dissectingmhcclassiiexportbcellmaturationanddmstabilitydefectsininvariantchainmutantmice
AT bikoffe dissectingmhcclassiiexportbcellmaturationanddmstabilitydefectsininvariantchainmutantmice