Preferential Th1 Immune Response in Invariant Chain-Deficient Mice

MHC class II molecules associate with the invariant chain (Ii) molecule during biosynthesis. Ii facilitates the folding of class II molecules, interferes with their peptide association, and is involved in MHC class II transport. In this study, we have investigated the in vitro and in vivo immune res...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2002-02, Vol.168 (4), p.1610-1617
Main Authors: Topilski, Ian, Harmelin, Alon, Flavell, Richard A, Levo, Yoram, Shachar, Idit
Format: Article
Language:English
Subjects:
Animals
Antigens, Differentiation, B-Lymphocyte - genetics
Antigens, Differentiation, B-Lymphocyte - physiology
Asthma - immunology
Asthma - pathology
CD4 antigen
Cells, Cultured
Colitis - immunology
Colitis - pathology
Cytokines - biosynthesis
Dose-Response Relationship, Drug
Histocompatibility Antigens Class II - genetics
Histocompatibility Antigens Class II - physiology
Hypersensitivity, Delayed - immunology
Lymphocyte Activation
Mice
Mice, Inbred C57BL
Mice, Knockout
Mitogens - pharmacology
Th1 Cells - immunology
Th2 Cells - immunology
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Summary:MHC class II molecules associate with the invariant chain (Ii) molecule during biosynthesis. Ii facilitates the folding of class II molecules, interferes with their peptide association, and is involved in MHC class II transport. In this study, we have investigated the in vitro and in vivo immune response of Ii-deficient mice (Ii(-/-)). Our results have demonstrated that CD4(+) T cells from Ii(-/-) mice proliferate normally in vitro after in vivo immunization with protein Ags. However, cytokine secretion profiles of Ag-primed CD4(+) T cells from Ii(-/-) mice differ from CD4(+) T cells from wild-type mice. Whereas cells from wild-type mice secrete IFN-gamma and IL-4, cells from Ii(-/-) mice secrete mostly IFN-gamma. Moreover, Ii(-/-) mice exhibit a normal Th1 response in the delayed-type hypersensitivity and trinitrobenzene sulfonic acid colitis models; however, these mice lack an in vivo Th2 response, as demonstrated in the asthma model. Therefore, we suggest that defective Ag presentation in Ii(-/-) mice leads selectively to a Th1 effector response.
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.168.4.1610