The Journal of Experimental Medicine
Avanti Polar Lipids, Inc.
  Home | Help | Feedback | Subscriptions | Archive | Search | Table of Contents

This Article
Right arrow Full Text
Right arrow Full Text (PDF, 306K)
Right arrow PPT slides of all figures
Right arrow Alert me when this article is cited
Right arrow Citation Map
Services
Right arrow Email this article
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new content in the JEM
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Colonna, M.
Right arrow Articles by López-Botet, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Colonna, M.
Right arrow Articles by López-Botet, M.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene*OMIM
*Protein*UniGene
*Compound via MeSH
*Substance via MeSH
Hazardous Substances DB
*CALCIUM COMPOUNDS
*CALCIUM, ELEMENTAL
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Facebook   Add to Reddit   Add to Technorati   Add to Twitter  
What's this?
© The Rockefeller University Press, 0022-1007/1997/12/1809/ $5.00
The Journal of Experimental Medicine, Volume 186, Number 11, December 1, 1997 1809-1818


Articles

A Common Inhibitory Receptor for Major Histocompatibility Complex Class I Molecules on Human Lymphoid and Myelomonocytic Cells

Marco Colonna*, Francisco Navarro{ddagger}, Teresa Bellón{ddagger}, Manuel Llano{ddagger}, Pilar García{ddagger}, Jacqueline Samaridis*, Lena Angman*, Marina Cella*, and Miguel López-Botet{ddagger}

From the * Basel Institute for Immunology, Basel CH-4005, Switzerland; and {ddagger} Hospital Universitario de la Princesa, 28006 Madrid, Spain

Natural killer (NK) cell–mediated lysis is negatively regulated by killer cell inhibitory receptors specific for major histocompatibility complex (MHC) class I molecules. In this study, we characterize a novel inhibitory MHC class I receptor of the immunoglobulin-superfamily, expressed not only by subsets of NK and T cells, but also by B cells, monocytes, macrophages, and dendritic cells. This receptor, called Ig-like transcript (ILT)2, binds MHC class I molecules and delivers a negative signal that inhibits killing by NK and T cells, as well as Ca2+ mobilization in B cells and myelomonocytic cells triggered through the B cell antigen receptor and human histocompatibility leukocyte antigens (HLA)–DR, respectively. In addition, myelomonocytic cells express receptors homologous to ILT2, which are characterized by extensive polymorphism and might recognize distinct HLA class I molecules. These results suggest that diverse leukocyte lineages have adopted recognition of self–MHC class I molecules as a common strategy to control cellular activation during an immune response.


Address correspondence to Marco Colonna, Basel Institute for Immunology, 487 Grenzacherstrasse, CH-4005 Basel, Switzerland. Phone: 41-61-605-1393; FAX: 41-61-605-1364; E-mail: colonna{at}bii.ch  or Miguel López-Botet, Servicio de Inmunología, Hospital de la Princesa, Diego de León 62, 28006 Madrid, Spain. Phone: 34-1-520-2370; FAX: 34-1-309-2496; E-mail: mlbotet/princesa{at}hup.es

The Basel Institute for Immunology was founded and is supported by Hoffmann-La Roche Ltd., Basel, Switzerland. The work at Hospital de la Princesa is supported by grants SAF96/0335 (Plan Nacional I+D) and PL950062 (European Commission). M. Llano is the recipient of a fellowship from the Fundacion Rich.

1 Abbreviations used in this paper: DC, dendritic cell; ILT, Ig-like transcript; ITIM, immunoreceptor tyrosine-based inhibitory motifs; KIR, killer cell inhibitory receptor; RBL, rat basophilic leukemia; rADCC, reverse antibody-dependent cell-mediated cytoxicity; SF, superfamily; TSST, toxic shock syndrome toxin.


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


This article has been cited by other articles:



  Home | Help | Feedback | Subscriptions | Archive | Search
TABLE OF CONTENTS