Abstract
The nonclassical histocompatibility class I gene HLA-G has a tissue-restricted expression. To explore mechanisms involved in HLA-G transcriptional regulation, we have investigated the effect of stress, including heat shock and arsenite treatment, on HLA-G expression in tumor cell lines. We show that stress induces an increase of the level of the different HLA-G alternative transcripts without affecting other MHC class I HLA-A, -B, -E, and -F transcripts. A heat shock element (HSE) that binds to heat shock factor 1 (HSF1) on stress conditions was further identified within the HLA-G promoter. Considering the ability of HLA-G to modulate the function of immunocompetent cells, we hypothesize a new feature of HLA-G as a signal regulating the immune response to stress.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Arsenites / pharmacology*
-
Blotting, Northern
-
Cloning, Molecular
-
DNA-Binding Proteins / genetics
-
DNA-Binding Proteins / metabolism*
-
Dactinomycin / pharmacology
-
Gene Expression Regulation* / drug effects
-
Genes, MHC Class I
-
HLA Antigens / genetics*
-
HLA Antigens / metabolism
-
HLA-G Antigens
-
HSP70 Heat-Shock Proteins / genetics
-
HSP70 Heat-Shock Proteins / metabolism
-
Heat Shock Transcription Factors
-
Heat-Shock Proteins / physiology*
-
Heat-Shock Response*
-
Histocompatibility Antigens Class I / genetics*
-
Histocompatibility Antigens Class I / metabolism
-
Humans
-
Male
-
Promoter Regions, Genetic / genetics*
-
RNA, Messenger / metabolism
-
Reverse Transcriptase Polymerase Chain Reaction
-
Transcription Factors
-
Tumor Cells, Cultured
Substances
-
Arsenites
-
DNA-Binding Proteins
-
HLA Antigens
-
HLA-G Antigens
-
HSF1 protein, human
-
HSP70 Heat-Shock Proteins
-
Heat Shock Transcription Factors
-
Heat-Shock Proteins
-
Histocompatibility Antigens Class I
-
RNA, Messenger
-
Transcription Factors
-
Dactinomycin