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 abolishin
g NK lysis, we studied HLA-G in a large panel of human tumour tissues and h
uman tumour cell lines of different origin that were previously characteriz
ed for HLA-A, -B, and -C expression. We studied HLA-G mRNA transcripts usin
g RT-PCR, and HLA-G1 expression by FAGS 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 t
wo specific monoclonal antibodies (mAbs) (87G and 01G). We cannot, however,
exclude the possibility that some isoforms other than HLA-G1 may be expres
sed in some tumours. (C) 1999 Elsevier Science Ireland Ltd. All rights rese
rved.