The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1999/4/1149/ $5.00
The Journal of Experimental Medicine, Volume 189, Number 7, April 5, 1999 1149-1156

Articles

Tetrameric Complexes of Human Histocompatibility Leukocyte Antigen (HLA)-G Bind to Peripheral Blood Myelomonocytic Cells

David S.J. Allan*, Marco Colonna{ddagger}, Lewis L. Lanier§, Tatyana D. Churakova§, John S. Abrams§, Shirley A. Ellis||, Andrew J. McMichael*, and Veronique M. Braud*

From the * Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, United Kingdom; {ddagger} Basel Institute for Immunology, Basel CH-4005, Switzerland; § DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, California 94304; and the || Institute for Animal Health, Compton RG20 7NN, United Kingdom

The nonclassical MHC class I molecule human histocompatibility leukocyte antigen (HLA)-G is selectively expressed on fetal trophoblast tissue at the maternal–fetal interface in pregnancy. It has long been suggested that HLA-G may inhibit maternal natural killer (NK) cells through interaction with particular NK cell receptors (KIRs). To investigate interactions of HLA-G, we constructed phycoerythrin-labeled tetrameric complexes of HLA-G refolded with a self-peptide. These HLA-G tetramers failed to bind to NK cells and cells transfected with CD94/NKG2 and killer immunoglobulin-like NK receptors. In contrast, HLA-G tetramers did bind to peripheral blood monocytes, staining a CD16+CD14mid subset with greater intensity. On transfectants, HLA-G tetramers bound to inhibitory immunoglobulin-like transcript (ILT)2 and ILT4 receptors. However, staining in the presence of antibodies reactive with ILT receptors revealed that the interaction of HLA-G tetramers with blood monocytes was largely due to binding to ILT4. These results suggest that the primary role of HLA-G may be the modulation of myelomonocytic cell behavior in pregnancy.

Key Words: immunoglobulin-like transcript • monocyte • natural killer cell • CD94 • killer immunoglobulin-like receptor

Address correspondence to Veronique M. Braud, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford OX3 9DS, UK. Phone: 44-1865-222-334; Fax: 44-1865-222-502; E-mail: vbraud{at}molbiol.ox.ac.uk

The authors gratefully acknowledge G. Ogg, J. Wilson, T. Dong, A. King, R. Allen, L. Tan, and P. Hansasuta for supplying tetramers of classical MHC class I molecules. We thank B. Corliss for making transfectants; T. McClanahan for cloning of ILT gene sequences; S. Zurawski for provision of recombinant ILT6 fusion proteins; and S. Gordon, J. Austyn, D. Chao, D. Mason, J. Cordell, D. Jackson, L. Moretta, A. King, and Y. Loke for antibodies and helpful discussions.

Abbreviations used: DC, dendritic cell; Tet, tetramer; ILT, immunoglobulin-like transcript; KIR, killer immunoglobulin-like receptor.


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