Enhanced B7-2 Gene Expression by Interferon-γ in Human Monocytic Cells Is Controlled Through Transcriptional and Posttranscriptional Mechanisms
B7-2 is a costimulatory molecule expressed on professional antigen-presenting cells that provides T cells with a critical signal resulting in T-cell activation. Interferon-γ (IFN-γ) enhances B7-2 protein expression in monocytic cells. However, the molecular mechanisms controlling the enhanced expres...
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| Published in | Blood Vol. 94; no. 5; pp. 1782 - 1789 |
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| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
01.09.1999
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| Online Access | Get full text |
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| Abstract | B7-2 is a costimulatory molecule expressed on professional antigen-presenting cells that provides T cells with a critical signal resulting in T-cell activation. Interferon-γ (IFN-γ) enhances B7-2 protein expression in monocytic cells. However, the molecular mechanisms controlling the enhanced expression of B7-2 are poorly understood. Northern blot and flow cytometry analysis revealed that human monocytes and the human monocytic cell line MonoMac6 (MM6) constitutively expressed B7-2 mRNA and protein and IFN-γ treatment further enhanced the expression of both molecules. The ability of IFN-γ to enhance B7-2 mRNA was evident at the dose of 31 U/mL and reached plateau levels at 500 U/mL. The effects of IFN-γ on B7-2 mRNA expression were time dependent and occurred within 3 hours of treatment and increased through 24 hours. In vitro transcription assays and mRNA stability experiments showed that IFN-γ increases both transcriptional activity and the stability of B7-2 mRNA. Treatment of MM6 cells with cycloheximide showed that de novo protein synthesis was not required for the IFN-γ–enhanced expression of B7-2 mRNA. Overall, these studies show for the first time that IFN-γ–enhanced expression of B7-2 protein in human monocytic cells is controlled at the gene level through a dual mechanism involving transcriptional and posttranscriptional mechanisms. |
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| AbstractList | B7-2 is a costimulatory molecule expressed on professional antigen-presenting cells that provides T cells with a critical signal resulting in T-cell activation. Interferon-γ (IFN-γ) enhances B7-2 protein expression in monocytic cells. However, the molecular mechanisms controlling the enhanced expression of B7-2 are poorly understood. Northern blot and flow cytometry analysis revealed that human monocytes and the human monocytic cell line MonoMac6 (MM6) constitutively expressed B7-2 mRNA and protein and IFN-γ treatment further enhanced the expression of both molecules. The ability of IFN-γ to enhance B7-2 mRNA was evident at the dose of 31 U/mL and reached plateau levels at 500 U/mL. The effects of IFN-γ on B7-2 mRNA expression were time dependent and occurred within 3 hours of treatment and increased through 24 hours. In vitro transcription assays and mRNA stability experiments showed that IFN-γ increases both transcriptional activity and the stability of B7-2 mRNA. Treatment of MM6 cells with cycloheximide showed that de novo protein synthesis was not required for the IFN-γ–enhanced expression of B7-2 mRNA. Overall, these studies show for the first time that IFN-γ–enhanced expression of B7-2 protein in human monocytic cells is controlled at the gene level through a dual mechanism involving transcriptional and posttranscriptional mechanisms. |
| Author | Garcia, C.S. Bosco, M.C. Curiel, R.E. Rottschafer, S. Espinoza-Delgado, I. |
| Author_xml | – sequence: 1 givenname: R.E. surname: Curiel fullname: Curiel, R.E. organization: From Department of Medicine and Stanley S. Scott Cancer Center, Louisiana State University Medical Center, New Orleans, LA; and Laboratorio di Biologia Molecolare, Instituto Giannina Gaslini, Genova Quarto, Italy – sequence: 2 givenname: C.S. surname: Garcia fullname: Garcia, C.S. organization: From Department of Medicine and Stanley S. Scott Cancer Center, Louisiana State University Medical Center, New Orleans, LA; and Laboratorio di Biologia Molecolare, Instituto Giannina Gaslini, Genova Quarto, Italy – sequence: 3 givenname: S. surname: Rottschafer fullname: Rottschafer, S. organization: From Department of Medicine and Stanley S. Scott Cancer Center, Louisiana State University Medical Center, New Orleans, LA; and Laboratorio di Biologia Molecolare, Instituto Giannina Gaslini, Genova Quarto, Italy – sequence: 4 givenname: M.C. surname: Bosco fullname: Bosco, M.C. organization: From Department of Medicine and Stanley S. Scott Cancer Center, Louisiana State University Medical Center, New Orleans, LA; and Laboratorio di Biologia Molecolare, Instituto Giannina Gaslini, Genova Quarto, Italy – sequence: 5 givenname: I. surname: Espinoza-Delgado fullname: Espinoza-Delgado, I. organization: From Department of Medicine and Stanley S. Scott Cancer Center, Louisiana State University Medical Center, New Orleans, LA; and Laboratorio di Biologia Molecolare, Instituto Giannina Gaslini, Genova Quarto, Italy |
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