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dc.contributor.authorCromme, F V
dc.contributor.authorAirey, J
dc.contributor.authorHeemels, M T
dc.contributor.authorPloegh, H L
dc.contributor.authorKeating, P J
dc.contributor.authorStern, Peter L
dc.contributor.authorMeijer, C J
dc.contributor.authorWalboomers, J M
dc.date.accessioned2010-04-09T10:51:17Z
dc.date.available2010-04-09T10:51:17Z
dc.date.issued1994-01-01
dc.identifier.citationLoss of transporter protein, encoded by the TAP-1 gene, is highly correlated with loss of HLA expression in cervical carcinomas. 1994, 179 (1):335-40 J. Exp. Med.en
dc.identifier.issn0022-1007
dc.identifier.pmid8270878
dc.identifier.urihttp://hdl.handle.net/10541/96118
dc.description.abstractMalignant tumor cells can escape CD8+ cytotoxic T cell killing by downregulating class I major histocompatibility complex (MHC) expression. Stable class I MHC surface expression requires loading of the heavy chain/light chain dimer with antigenic peptide, which is delivered to class I MHC molecules in the endoplasmic reticulum by the presumed peptide transporter, encoded by the transporter associated with antigen presentation (TAP) 1 and 2 genes. We have investigated whether loss of class I MHC expression frequently observed in different cancers could result from interference with TAP function. A polyclonal antiserum, raised against a bacterial glutathione S-transferase/human TAP-1 fusion protein, was used for the immunohistochemical analysis of TAP-1 expression in 76 cervical carcinomas. Results showed loss of TAP-1 expression in neoplastic cells in 37 out of 76 carcinomas. Immunohistochemical double staining procedures in combination with HLA-specific antibodies revealed congruent loss at the single cell level of TAP-1 and HLA-A/B expression in 28 out of 37 carcinomas. The remaining samples expressed HLA(-A) in the absence of TAP-1 (n = 6) or showed loss of HLA(-A/B) while TAP-1 was expressed (n = 3). These data strongly indicate that inhibition of peptide transport by downregulation of TAP-1 is a potential strategy of malignant cells to evade immune surveillance.
dc.language.isoenen
dc.subjectUterine Cervical Canceren
dc.subject.meshATP-Binding Cassette Transporters
dc.subject.meshAntibody Specificity
dc.subject.meshBiological Transport
dc.subject.meshCarrier Proteins
dc.subject.meshFemale
dc.subject.meshHLA Antigens
dc.subject.meshHistocompatibility Antigens Class I
dc.subject.meshHistocompatibility Antigens Class II
dc.subject.meshHumans
dc.subject.meshImmune Sera
dc.subject.meshUterine Cervical Neoplasms
dc.titleLoss of transporter protein, encoded by the TAP-1 gene, is highly correlated with loss of HLA expression in cervical carcinomas.en
dc.typeArticleen
dc.contributor.departmentDepartment of Pathology, Free University Hospital, Amsterdam, The Netherlands.en
dc.identifier.journalThe Journal of Experimental Medicineen
html.description.abstractMalignant tumor cells can escape CD8+ cytotoxic T cell killing by downregulating class I major histocompatibility complex (MHC) expression. Stable class I MHC surface expression requires loading of the heavy chain/light chain dimer with antigenic peptide, which is delivered to class I MHC molecules in the endoplasmic reticulum by the presumed peptide transporter, encoded by the transporter associated with antigen presentation (TAP) 1 and 2 genes. We have investigated whether loss of class I MHC expression frequently observed in different cancers could result from interference with TAP function. A polyclonal antiserum, raised against a bacterial glutathione S-transferase/human TAP-1 fusion protein, was used for the immunohistochemical analysis of TAP-1 expression in 76 cervical carcinomas. Results showed loss of TAP-1 expression in neoplastic cells in 37 out of 76 carcinomas. Immunohistochemical double staining procedures in combination with HLA-specific antibodies revealed congruent loss at the single cell level of TAP-1 and HLA-A/B expression in 28 out of 37 carcinomas. The remaining samples expressed HLA(-A) in the absence of TAP-1 (n = 6) or showed loss of HLA(-A/B) while TAP-1 was expressed (n = 3). These data strongly indicate that inhibition of peptide transport by downregulation of TAP-1 is a potential strategy of malignant cells to evade immune surveillance.


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