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4 - Control of MHC class I gene expression

Published online by Cambridge University Press:  11 September 2009

Keiko Ozato
Affiliation:
National Institute of Child Health and Human Development, Bethesda
G. Eric Blair
Affiliation:
University of Leeds
Craig R. Pringle
Affiliation:
University of Warwick
D. John Maudsley
Affiliation:
University of Warwick
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Summary

Introduction

This chapter deals with transcriptional regulation of MHC class I genes in normal physiology and development. The main focus is transcription factors involved in regulating class I gene expression and the mechanism of action of these factors.

Class I genes are widely expressed in many adult tissues. However, levels of class I expression vary among different tissues; some tissues do not express class I genes at a significant level (Klein, 1975). While lymphoid tissues express class I genes at high levels, there is virtually no expression in the CNS. The lack of class I gene expression in the CNS constitutes a unique immunological environment, which accounts for persistent infection by some viruses (Joly, Mucke & Oldstone, 1991). Other tissues, such as pancreas and muscle, appear to be low in class I gene expression (David-Watine, Israel & Kourilsky, 1990a). Class I gene expression is developmentally controlled: class I mRNAs are not found until mouse embryos reach mid-somite stage (Ozato, Wan & Orrison, 1985). Levels of MHC class I expression in embryonic tissues vary but are higher in haemato/lymphopoietic tissues than in other tissues (Hedley et al, 1989). Class I mRNA levels rise sharply during the first week of neonatal development in the mouse (Kasik, Wan & Ozato, 1987). So far, the molecule responsible for the primary onset of class I expression during embryogenesis, or that which triggers the second, post-natal upsurge of class I expression, has not been identified.

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Publisher: Cambridge University Press
Print publication year: 1995

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