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Mice deficient in invariant‐chain and MHC class II exhibit a normal mature B2 cell compartment
Author(s) -
Maehr Rene´,
Kraus Manfred,
Ploegh Hidde L.
Publication year - 2004
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.200425246
Subject(s) - biology , mhc class ii , cd74 , microbiology and biotechnology , mhc class i , b cell , cell , major histocompatibility complex , mhc restriction , mutant , t cell , genetics , antigen , immune system , gene , antibody
Abstract The role of the invariant chain (Ii), an MHC class II‐associated chaperone, in B cell development is controversial. Ii deficient mice (Ii –/– mice) show a defect in B cell development.This defect has been attributed to the absence of a fragment liberated from the Ii by intramembranous proteolysis. It was proposed that this fragment is required for activation of the NF‐κB pathway as a means of controlling B cell maturation. The opposing view holds that defects in the assembly of MHC class II molecules result in impaired B cell development. Here we demonstrate that a lack of Ii indeed causes defects in B cell development, with fewer mature B cells in the periphery as previously reported, but that in a compound‐mutant from which both Ii and all MHC class II subunits are absent, B cell development is normal. We suggest that neither Ii itself, nor the MHC class II products are required for normal B cell development.