Defective major histocompatibility complex class II assembly, transport, peptide acquisition, and CD4+ T cell selection in mice lacking invariant chain expression.
Author(s)
Type
Journal Article
Abstract
We used gene targeting techniques to produce mice lacking the invariant chain associated with major histocompatibility complex (MHC) class II molecules. Cells from these mice show a dramatic reduction in surface class II, resulting from both defective association of class II alpha and beta chains and markedly decreased post-Golgi transport. The few class II alpha/beta heterodimers reaching the cell surface behave as if empty or occupied by an easily displaced peptide, and display a distinct structure. Mutant spleen cells are defective in their ability to present intact protein antigens, but stimulate enhanced responses in the presence of peptides. These mutant mice have greatly reduced numbers of thymic and peripheral CD4+ T cells. Overall, this striking phenotype establishes that the invariant chain plays a critical role in regulating MHC class II expression and function in the intact animal.
Date Issued
1993-06-01
Date Acceptance
1993-06-01
Citation
Journal of Experimental Medicine, 1993, 177 (6), pp.1699-1712
ISSN
0022-1007
Publisher
Rockefeller University Press
Start Page
1699
End Page
1712
Journal / Book Title
Journal of Experimental Medicine
Volume
177
Issue
6
Copyright Statement
© 1993 The Author(s).
Identifier
https://www.ncbi.nlm.nih.gov/pubmed/8098731
Subjects
Animals
Antigens, Differentiation, B-Lymphocyte
Antigens, Surface
Biological Transport
CD4-Positive T-Lymphocytes
Cells, Cultured
Hematopoietic Stem Cells
Histocompatibility Antigens Class II
Mice
Mice, Inbred C57BL
Mutation
Peptide Fragments
Publication Status
Published
Coverage Spatial
United States
Date Publish Online
1993-06-01