Interferon-α induction of STATs1, -3 DNA binding and growth arrest is independent of Lck and active mitogen-activated kinase in T cells

Troy C. Lund; Maria M. Medveczky; Peter G. Medveczky

doi:10.1006/cimm.1999.1466

Interferon-α induction of STATs1, -3 DNA binding and growth arrest is independent of Lck and active mitogen-activated kinase in T cells

Troy C. Lund
, Maria M. Medveczky
, Peter G. Medveczky

Research output: Contribution to journal › Article › peer-review

11 Scopus citations

Abstract

Type I interferons (IFNs) are a family of cytokines that have antiviral and antiproliferative effects. Data regarding the processes by which these cytokines transduce signals from the cell membrane to the nucleus are becoming increasingly complex. The most characterized pathway is via JAK- STAT signaling. Previous studies established a potential role for the Src- family kinase Lck in JAK-STAT signaling. Therefore, this study was designed to analyze the role of Lck in IFN-α signaling by using the Jurkat, JCam (an Lck-defective cell line derived from Jurkat), and JCam/Lck (JCam cells with Lck restored). The results show that IFN-α can induce MAPK activity, but only in cells containing Lck. Furthermore, STATs1 and -3 are effectively phosphorylated and activated to bind DNA in the absence of Lck expression in IFN-α-treated cells. Finally, the results demonstrate that IFN-α exerts an antiproliferative effect in all three cell lines. These data indicate that Lck and active MAPK do not affect IFN-α-induced growth arrest or induction of STAT1s1 and -3 DNA binding ability.

Original language	English (US)
Pages (from-to)	133-139
Number of pages	7
Journal	Cellular Immunology
Volume	192
Issue number	2
DOIs	https://doi.org/10.1006/cimm.1999.1466
State	Published - Mar 15 1999
Externally published	Yes

Bibliographical note

Funding Information:
1This work was supported by U.S. Public Health Service Grants R01 CA 43264 and R01 CA 75895. 2To whom correspondence should be addressed at Department of Medical Microbiology and Immunology, University of South Florida, MDC 10, 12901 Bruce B. Downs Blvd., Tampa, FL 33612. Fax: 813-974-4151.

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This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Cytokines
Molecular biology
Signal transduction
T lymphocytes

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10.1006/cimm.1999.1466

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title = "Interferon-α induction of STATs1, -3 DNA binding and growth arrest is independent of Lck and active mitogen-activated kinase in T cells",

abstract = "Type I interferons (IFNs) are a family of cytokines that have antiviral and antiproliferative effects. Data regarding the processes by which these cytokines transduce signals from the cell membrane to the nucleus are becoming increasingly complex. The most characterized pathway is via JAK- STAT signaling. Previous studies established a potential role for the Src- family kinase Lck in JAK-STAT signaling. Therefore, this study was designed to analyze the role of Lck in IFN-α signaling by using the Jurkat, JCam (an Lck-defective cell line derived from Jurkat), and JCam/Lck (JCam cells with Lck restored). The results show that IFN-α can induce MAPK activity, but only in cells containing Lck. Furthermore, STATs1 and -3 are effectively phosphorylated and activated to bind DNA in the absence of Lck expression in IFN-α-treated cells. Finally, the results demonstrate that IFN-α exerts an antiproliferative effect in all three cell lines. These data indicate that Lck and active MAPK do not affect IFN-α-induced growth arrest or induction of STAT1s1 and -3 DNA binding ability.",

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note = "Funding Information: 1This work was supported by U.S. Public Health Service Grants R01 CA 43264 and R01 CA 75895. 2To whom correspondence should be addressed at Department of Medical Microbiology and Immunology, University of South Florida, MDC 10, 12901 Bruce B. Downs Blvd., Tampa, FL 33612. Fax: 813-974-4151.",

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AU - Lund, Troy C.

AU - Medveczky, Maria M.

AU - Medveczky, Peter G.

N1 - Funding Information: 1This work was supported by U.S. Public Health Service Grants R01 CA 43264 and R01 CA 75895. 2To whom correspondence should be addressed at Department of Medical Microbiology and Immunology, University of South Florida, MDC 10, 12901 Bruce B. Downs Blvd., Tampa, FL 33612. Fax: 813-974-4151.

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N2 - Type I interferons (IFNs) are a family of cytokines that have antiviral and antiproliferative effects. Data regarding the processes by which these cytokines transduce signals from the cell membrane to the nucleus are becoming increasingly complex. The most characterized pathway is via JAK- STAT signaling. Previous studies established a potential role for the Src- family kinase Lck in JAK-STAT signaling. Therefore, this study was designed to analyze the role of Lck in IFN-α signaling by using the Jurkat, JCam (an Lck-defective cell line derived from Jurkat), and JCam/Lck (JCam cells with Lck restored). The results show that IFN-α can induce MAPK activity, but only in cells containing Lck. Furthermore, STATs1 and -3 are effectively phosphorylated and activated to bind DNA in the absence of Lck expression in IFN-α-treated cells. Finally, the results demonstrate that IFN-α exerts an antiproliferative effect in all three cell lines. These data indicate that Lck and active MAPK do not affect IFN-α-induced growth arrest or induction of STAT1s1 and -3 DNA binding ability.

AB - Type I interferons (IFNs) are a family of cytokines that have antiviral and antiproliferative effects. Data regarding the processes by which these cytokines transduce signals from the cell membrane to the nucleus are becoming increasingly complex. The most characterized pathway is via JAK- STAT signaling. Previous studies established a potential role for the Src- family kinase Lck in JAK-STAT signaling. Therefore, this study was designed to analyze the role of Lck in IFN-α signaling by using the Jurkat, JCam (an Lck-defective cell line derived from Jurkat), and JCam/Lck (JCam cells with Lck restored). The results show that IFN-α can induce MAPK activity, but only in cells containing Lck. Furthermore, STATs1 and -3 are effectively phosphorylated and activated to bind DNA in the absence of Lck expression in IFN-α-treated cells. Finally, the results demonstrate that IFN-α exerts an antiproliferative effect in all three cell lines. These data indicate that Lck and active MAPK do not affect IFN-α-induced growth arrest or induction of STAT1s1 and -3 DNA binding ability.

KW - Cytokines

KW - Molecular biology

KW - Signal transduction

KW - T lymphocytes

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Interferon-α induction of STATs1, -3 DNA binding and growth arrest is independent of Lck and active mitogen-activated kinase in T cells

Abstract

Bibliographical note

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