http://www.cnr.it/ontology/cnr/individuo/prodotto/ID12183

Defective class II transactivator expression in a B lymphoma cell line (Articolo in rivista)

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Defective class II transactivator expression in a B lymphoma cell line (Articolo in rivista) (literal)

Anno

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Alternative label

T Prod'homme 1, B Drenou 2, C De Ruyffelaere 1, G Barbieri 1, W Wiszniewski 3, C Bastard 4, D Charron 1 and C Alcaide-Loridan 1 (2004)
Defective class II transactivator expression in a B lymphoma cell line
in Leukemia; NATURE PUBLISHING GROUP,, LONDON (Regno Unito)
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

T Prod'homme 1, B Drenou 2, C De Ruyffelaere 1, G Barbieri 1, W Wiszniewski 3, C Bastard 4, D Charron 1 and C Alcaide-Loridan 1 (literal)

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1 INSERM U396, Centre de Recherches Biomedicales des Cordeliers, Paris, France; 2 CHU, Service d'Hematologie-Immunologie, Rennes, France; 3 Department of Medical Genetics, Institute of Mother and Child, Warsaw, Poland; 4 Laboratoire de GenetiqueOncologique, Centre Henri-Becquerel, Rouen, France (literal)

Titolo

Defective class II transactivator expression in a B lymphoma cell line (literal)

Abstract

Loss of MHC class II expression in B-cell lymphoma has been associated with a higher tumorigenicity resulting from lower titers of tumor-infiltrating lymphocytes. This report aims towards the identification of the molecular mechanism leading to defective MHC class II expression in a B-cell lymphoma cell line, Rec-1. We evidenced a coordinated alteration of HLA-D gene transcription, reminiscent of B lymphoblastoid cell lines from patients with MHC class II deficiency. Genetic complementation performed between these cell lines and the lymphoma cells indicated that Rec-1 is altered in the MHC2TA gene. MHC2TA encodes the class II transactivator (CIITA), the master regulator of HLA-D gene expression. However, the coding sequence of the Rec-1 CIITA transcript did not reveal any mutation that could hamper the activity of the encoded protein. In agreement with the genetic complementation analysis, we evidenced a highly residual CIITA protein expression in the Rec-1 cell line resulting from a transcriptional defect affecting MHC2TA expression. Anti-HLA-DR monoclonal antibody treatment has proved efficient in the destruction of B lymphoma cells. Our data indicate that the appearance of variants losing CIITA, and thereby HLA-DR, expression will require a thorough monitoring during such immunotherapy protocols. (literal)

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