MHC class II-deficient tumor cell lines with a defective expression of the class II transactivator

Rodrigo Naves, Ana Maria Lennon, Giovanna Barbieri, Lilian Reyes, Gisella Puga, Laura Salas, Virginie Deffrennes, Mario Rosemblatt, Marc Fellous, Dominique Charron, Catherine Alcaïde-Loridan, Maria Rosa Bono

Resultado de la investigación: Article

11 Citas (Scopus)

Resumen

MHC class II expression defects have been evidenced in several human tumor cell lines originating from lung cancers or retinoblastoma. Accordingly, the mouse adenocarcinoma and fibrosarcoma cell lines, RAG and L(tk-), do not express I-A and I-E molecules even when treated with IFN-γ. Here we show that fusion of both cell lines restores the inducible expression of MHC class II, thereby demonstrating that they present different and recessive alterations outside the MHC class II locus. CIITA, the MHC class II transactivator, controls the tissue-specific expression of MHC class II genes and creates the architecture of the transcriptional complex that binds to the MHC class II gene promoters. In L(tk-) cells, C2ta transcripts, expressed from the gene encoding CIITA, were indeed detected in severely limited amounts, with a defect in C2ta transcription initiation. In agreement we show here that the L(tk-) cell line does not express the CIITA protein. In contrast, in the RAG cell line, C2ta transcripts were expressed at normal levels, from the proper initiation site. The nucleotide sequencing of the CIITA cDNA from RAG did not reveal any mutation. However, the CIITA protein was not detected. These data evidence a new type of defect in a MHC class II-defective tumor cell line, as we show here that the alteration in the RAG cells occurs downstream of C2ta transcription. The RAG mutation might therefore reside in the C2ta transcript nuclear export or translation, or in the stability of the CIITA protein.

Idioma originalEnglish
Páginas (desde-hasta)481-491
Número de páginas11
PublicaciónInternational Immunology
Volumen14
N.º5
DOI
EstadoPublished - 1 ene 2002

Huella dactilar

Tumor Cell Line
Cell Line
MHC Class II Genes
Mutation
Cell Nucleus Active Transport
Retinoblastoma
Protein Stability
Fibrosarcoma
Lung Neoplasms
Proteins
Adenocarcinoma
Nucleotides
Complementary DNA
MHC class II transactivator protein
Genes

ASJC Scopus subject areas

  • Immunology

Citar esto

Naves, R., Lennon, A. M., Barbieri, G., Reyes, L., Puga, G., Salas, L., ... Bono, M. R. (2002). MHC class II-deficient tumor cell lines with a defective expression of the class II transactivator. International Immunology, 14(5), 481-491. https://doi.org/10.1093/intimm/14.5.481
Naves, Rodrigo ; Lennon, Ana Maria ; Barbieri, Giovanna ; Reyes, Lilian ; Puga, Gisella ; Salas, Laura ; Deffrennes, Virginie ; Rosemblatt, Mario ; Fellous, Marc ; Charron, Dominique ; Alcaïde-Loridan, Catherine ; Bono, Maria Rosa. / MHC class II-deficient tumor cell lines with a defective expression of the class II transactivator. En: International Immunology. 2002 ; Vol. 14, N.º 5. pp. 481-491.
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abstract = "MHC class II expression defects have been evidenced in several human tumor cell lines originating from lung cancers or retinoblastoma. Accordingly, the mouse adenocarcinoma and fibrosarcoma cell lines, RAG and L(tk-), do not express I-A and I-E molecules even when treated with IFN-γ. Here we show that fusion of both cell lines restores the inducible expression of MHC class II, thereby demonstrating that they present different and recessive alterations outside the MHC class II locus. CIITA, the MHC class II transactivator, controls the tissue-specific expression of MHC class II genes and creates the architecture of the transcriptional complex that binds to the MHC class II gene promoters. In L(tk-) cells, C2ta transcripts, expressed from the gene encoding CIITA, were indeed detected in severely limited amounts, with a defect in C2ta transcription initiation. In agreement we show here that the L(tk-) cell line does not express the CIITA protein. In contrast, in the RAG cell line, C2ta transcripts were expressed at normal levels, from the proper initiation site. The nucleotide sequencing of the CIITA cDNA from RAG did not reveal any mutation. However, the CIITA protein was not detected. These data evidence a new type of defect in a MHC class II-defective tumor cell line, as we show here that the alteration in the RAG cells occurs downstream of C2ta transcription. The RAG mutation might therefore reside in the C2ta transcript nuclear export or translation, or in the stability of the CIITA protein.",
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Naves, R, Lennon, AM, Barbieri, G, Reyes, L, Puga, G, Salas, L, Deffrennes, V, Rosemblatt, M, Fellous, M, Charron, D, Alcaïde-Loridan, C & Bono, MR 2002, 'MHC class II-deficient tumor cell lines with a defective expression of the class II transactivator', International Immunology, vol. 14, n.º 5, pp. 481-491. https://doi.org/10.1093/intimm/14.5.481

MHC class II-deficient tumor cell lines with a defective expression of the class II transactivator. / Naves, Rodrigo; Lennon, Ana Maria; Barbieri, Giovanna; Reyes, Lilian; Puga, Gisella; Salas, Laura; Deffrennes, Virginie; Rosemblatt, Mario; Fellous, Marc; Charron, Dominique; Alcaïde-Loridan, Catherine; Bono, Maria Rosa.

En: International Immunology, Vol. 14, N.º 5, 01.01.2002, p. 481-491.

Resultado de la investigación: Article

TY - JOUR

T1 - MHC class II-deficient tumor cell lines with a defective expression of the class II transactivator

AU - Naves, Rodrigo

AU - Lennon, Ana Maria

AU - Barbieri, Giovanna

AU - Reyes, Lilian

AU - Puga, Gisella

AU - Salas, Laura

AU - Deffrennes, Virginie

AU - Rosemblatt, Mario

AU - Fellous, Marc

AU - Charron, Dominique

AU - Alcaïde-Loridan, Catherine

AU - Bono, Maria Rosa

PY - 2002/1/1

Y1 - 2002/1/1

N2 - MHC class II expression defects have been evidenced in several human tumor cell lines originating from lung cancers or retinoblastoma. Accordingly, the mouse adenocarcinoma and fibrosarcoma cell lines, RAG and L(tk-), do not express I-A and I-E molecules even when treated with IFN-γ. Here we show that fusion of both cell lines restores the inducible expression of MHC class II, thereby demonstrating that they present different and recessive alterations outside the MHC class II locus. CIITA, the MHC class II transactivator, controls the tissue-specific expression of MHC class II genes and creates the architecture of the transcriptional complex that binds to the MHC class II gene promoters. In L(tk-) cells, C2ta transcripts, expressed from the gene encoding CIITA, were indeed detected in severely limited amounts, with a defect in C2ta transcription initiation. In agreement we show here that the L(tk-) cell line does not express the CIITA protein. In contrast, in the RAG cell line, C2ta transcripts were expressed at normal levels, from the proper initiation site. The nucleotide sequencing of the CIITA cDNA from RAG did not reveal any mutation. However, the CIITA protein was not detected. These data evidence a new type of defect in a MHC class II-defective tumor cell line, as we show here that the alteration in the RAG cells occurs downstream of C2ta transcription. The RAG mutation might therefore reside in the C2ta transcript nuclear export or translation, or in the stability of the CIITA protein.

AB - MHC class II expression defects have been evidenced in several human tumor cell lines originating from lung cancers or retinoblastoma. Accordingly, the mouse adenocarcinoma and fibrosarcoma cell lines, RAG and L(tk-), do not express I-A and I-E molecules even when treated with IFN-γ. Here we show that fusion of both cell lines restores the inducible expression of MHC class II, thereby demonstrating that they present different and recessive alterations outside the MHC class II locus. CIITA, the MHC class II transactivator, controls the tissue-specific expression of MHC class II genes and creates the architecture of the transcriptional complex that binds to the MHC class II gene promoters. In L(tk-) cells, C2ta transcripts, expressed from the gene encoding CIITA, were indeed detected in severely limited amounts, with a defect in C2ta transcription initiation. In agreement we show here that the L(tk-) cell line does not express the CIITA protein. In contrast, in the RAG cell line, C2ta transcripts were expressed at normal levels, from the proper initiation site. The nucleotide sequencing of the CIITA cDNA from RAG did not reveal any mutation. However, the CIITA protein was not detected. These data evidence a new type of defect in a MHC class II-defective tumor cell line, as we show here that the alteration in the RAG cells occurs downstream of C2ta transcription. The RAG mutation might therefore reside in the C2ta transcript nuclear export or translation, or in the stability of the CIITA protein.

KW - CIITA

KW - MHC class II

KW - Transcription

KW - Tumor cell line

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DO - 10.1093/intimm/14.5.481

M3 - Article

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JO - International Immunology

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