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Expression of HLA G in human tumors is not a frequent event
Author(s) -
Miguel Real Luis,
Cabrera Teresa,
Collado Antonia,
Jimenez Pilar,
Garcia Angel,
RuizCabello Francisco,
Garrido Federico
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19990517)81:4<512::aid-ijc2>3.0.co;2-o
Subject(s) - human leukocyte antigen , event (particle physics) , expression (computer science) , biology , medicine , immunology , genetics , antigen , computer science , physics , quantum mechanics , programming language
Expression of HLA G may be a way for tumor cells to escape immuno‐surveillance. HLA G is selectively expressed by extravillous trophoblast in the human placenta, a tissue that does not express HLA A or B molecules. It is tempting to propose that tumor cells resemble this unique HLA class I phenotype as they frequently lose classical HLA A, B and C class I expression. Such peculiar HLA class I distribution would in theory allow tumor cells to escape from T‐ and NK‐cell cytotoxicity. To determine whether HLA G is expressed on tumor cells, we studied HLA G mRNA levels using RT‐PCR and HLA G cell‐surface expression by immuno‐histological techniques in a panel of 50 human solid tumor tissues, 31 tumor cell lines of different origin, 4 autologous mucosa samples and 3 peripheral white cell samples. We found mRNA transcripts of different HLA G isoforms in most of the samples studied. However, we did not detect cell‐surface expression of HLA G using 3 specific monoclonal antibodies (MAbs; 87G, 01G and G223). HLA G was detected only in the U937 myelomonocytic cell line after stimulation with IFN‐γ. We favor the hypothesis that HLA G plays a minor role, if any, in providing an inhibitory signal to NK cells to escape immunosurveillance. We cannot, however, exclude the possibility that some other HLA G isoforms may be expressed in some tumors. Int. J. Cancer 81:512–518, 1999. © 1999 Wiley‐Liss, Inc.