Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article Full Text Full Text (PDF, 712K) PPT slides of all figures Alert me when this article is cited Citation Map Services Email this article Similar articles in this journal Similar articles in PubMed Alert me to new content in the JEM Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Waldburger, J.-M. Articles by Reith, W. Search for Related Content PubMed PubMed Citation Articles by Waldburger, J.-M. Articles by Reith, W. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Substance via MeSH Social Bookmarking                            What's this?

Original Article

^a Department of Genetics and Microbiology, University of Geneva Medical School, 1211 Geneva 4, Switzerland
^b Section of Clinical Immunology, University Hospital, 8044 Zurich, Switzerland
^c Ludwig Institute for Cancer Research, Lausanne Branch, and Institute of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland
Department of Genetics and Microbiology, University of Geneva Medical School, CMU, 1 rue Michel-Servet, 1211 Geneva 4, Switzerland.41-22-702-57-0241-22-702-56-66

walter.reith{at}medecine.unige.ch

MHC class II (MHCII) molecules play a pivotal role in the induction and regulation of immune responses. The transcriptional coactivator class II transactivator (CIITA) controls MHCII expression. The CIITA gene is regulated by three independent promoters (pI, pIII, pIV). We have generated pIV knockout mice. These mice exhibit selective abrogation of interferon (IFN)-–induced MHCII expression on a wide variety of non-bone marrow–derived cells, including endothelia, epithelia, astrocytes, and fibroblasts. Constitutive MHCII expression on cortical thymic epithelial cells, and thus positive selection of CD4⁺ T cells, is also abolished. In contrast, constitutive and inducible MHCII expression is unaffected on professional antigen-presenting cells, including B cells, dendritic cells, and IFN-–activated cells of the macrophage lineage. pIV^–/– mice have thus allowed precise definition of CIITA pIV usage in vivo. Moreover, they represent a unique animal model for studying the significance and contribution of MHCII-mediated antigen presentation by nonprofessional antigen-presenting cells in health and disease.

Key Words: knockout • promoter region • antigen-presenting cells • gene expression regulation • thymic selection

Abbreviations used in this paper: CIITA, class II transactivator; CNS, central nervous system; cTECs, cortical thymic epithelial cells; DCs, dendritic cells; ES, embryonic stem; MEFs, mouse embryonic fibroblasts; MHCI, MHC class I; MHCII, MHC class II.

© 2001 The Rockefeller University Press

CiteULike    Complore    Connotea    Del.icio.us    Digg    Facebook    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

• Honey, K., Rudensky, A. (2001). The Piv-Otal Class II Transactivator Promoter Regulates Major Histocompatibility Complex Class II Expression in the Thymus. JEM 194: f15-f18 [Full Text]  

Home | Help | Feedback | Subscriptions | Archive | Search

TABLE OF CONTENTS