Send to

Choose Destination
See comment in PubMed Commons below
FASEB J. 2005 Apr;19(6):662-4. Epub 2005 Jan 24.

HLA-G up-regulates ILT2, ILT3, ILT4, and KIR2DL4 in antigen presenting cells, NK cells, and T cells.

Author information

Service de Recherches en Hémato-Immunologie, Commissariat à L'Energie Atomique-DRM-DSV, Institut Universitaire d'Hématologie, Hôpital Saint Louis, Paris, France.


The nonclassical HLA class I antigen HLA-G is an inhibitory molecule involved in immune tolerance and immune escape. HLA-G exerts its inhibitory functions via interaction with inhibitory receptors ILT2, ILT4, and KIR2DL4, differentially expressed by NK, T, and antigen-presenting cells. Cells expressing HLA-G and cells expressing its receptors are often found in the vicinity of each other, but the mechanisms responsible for this colocalization are still unknown. We report that ILT2, ILT3, ILT4, and KIR2DL4 expression is up-regulated by HLA-G in antigen-presenting cells, NK cells, and T cells. Because this up-regulation seems not to require antigenic costimulation, it might precede an immune response. Functionally, up-regulation of inhibitory receptors in immune cells before stimulation might increase their activation thresholds and participate in immune escape mechanisms.

[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire
    Loading ...
    Support Center