Looking for HLA-G expression in human tumours.
Tumour and virus infected cells escape CTLs responses by losing some or all HLA class I molecules. However the NK escape mechanism that uses the HLA-A, -B, and -C tumour deficient variants is unknown. To determine whether HLA-G is expressed on tumour cells and thus favours tumour escape by abolishing NK lysis, we studied HLA-G in a large panel of human tumour tissues and human tumour cell lines of different origin that were previously characterized for HLA-A, -B, and -C expression. We studied HLA-G mRNA transcripts using RT-PCR, and HLA-G1 expression by FACS and immunohistochemical techniques. We found several mRNA transcripts of HLA-G isoforms in most of the samples studied. However, we detected no cell surface expression of HLA-G1 using two specific monoclonal antibodies (mAbs) (87G and 01G). We cannot, however, exclude the possibility that some isoforms other than HLA-G1 may be expressed in some tumours.
Real
L M
LM
Departamento de Análisis Clínicos, Hospital Universitario Virgen de las Nieves, Granada, Spain.
Cabrera
T
T
Canton
J
J
Oliva
R
R
Ruiz-Cabello
F
F
Garrido
F
F
D015870:Gene Expression; D006680:HLA Antigens / Q000096:biosynthesis* / Q000235:genetics; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000096:biosynthesis* / Q000235:genetics; D006801:Humans; D009369:Neoplasms / Q000235:genetics / Q000276:immunology*; D014407:Tumor Cells, Cultured
D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I