The gamma subunit of the interleukin-2 receptor is expressed in human monocytes and modulated by interleukin-2, interferon gamma, and transforming growth factor beta 1

Abstract The interleukin-2 receptor gamma (IL-2R gamma) chain is a newly recognized component of the IL-2R of lymphoid cells that is required for their response to IL-2. We investigated the expression of IL-2R gamma protein in human monocytes by Western blot analysis using an antiserum specific for IL-2R gamma. We found that IL-2R gamma subunit is constitutively expressed in human monocytes and upregulated by the monocyte-activating factors IL-2 and interferon gamma (IFN gamma). Furthermore, we show that transforming growth factor beta 1 (TGF beta 1) downmodulates, in a dose-dependent manner, basal and IL-2-induced, but not IFN gamma-induced, IL-2R gamma chain expression, and this effect may be responsible for TGF beta 1 suppressive activity on IL-2- activated monocytes. Overall, these results show that the expression of the IL-2R gamma subunit in human monocytes is tightly regulated by the cytokine network, suggesting a critical role played by this protein on monocyte activation.

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The gamma subunit of the interleukin-2 receptor is expressed in human monocytes and modulated by interleukin-2, interferon gamma, and transforming growth factor beta 1

Blood ◽

10.1182/blood.v83.12.3462.bloodjournal83123462 ◽

1994 ◽

Vol 83 (12) ◽

pp. 3462-3467 ◽

Cited By ~ 1

Author(s):

MC Bosco ◽

I Espinoza-Delgado ◽

M Schwabe ◽

SM Russell ◽

WJ Leonard ◽

...

Keyword(s):

Growth Factor ◽

Interferon Gamma ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Interleukin 2 ◽

Human Monocytes ◽

Gamma Chain ◽

Ifn Gamma ◽

Gamma Subunit ◽

Growth Factor Beta

The interleukin-2 receptor gamma (IL-2R gamma) chain is a newly recognized component of the IL-2R of lymphoid cells that is required for their response to IL-2. We investigated the expression of IL-2R gamma protein in human monocytes by Western blot analysis using an antiserum specific for IL-2R gamma. We found that IL-2R gamma subunit is constitutively expressed in human monocytes and upregulated by the monocyte-activating factors IL-2 and interferon gamma (IFN gamma). Furthermore, we show that transforming growth factor beta 1 (TGF beta 1) downmodulates, in a dose-dependent manner, basal and IL-2-induced, but not IFN gamma-induced, IL-2R gamma chain expression, and this effect may be responsible for TGF beta 1 suppressive activity on IL-2- activated monocytes. Overall, these results show that the expression of the IL-2R gamma subunit in human monocytes is tightly regulated by the cytokine network, suggesting a critical role played by this protein on monocyte activation.

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Cellular mRNA expression of interferon-gamma (IFN-gamma), IL-4 and transforming growth factor-beta (TGF-beta) in rats nasally tolerized against experimental autoimmune myasthenia gravis (EAMG)

Clinical & Experimental Immunology ◽

10.1046/j.1365-2249.1996.50755.x ◽

1996 ◽

Vol 104 (3) ◽

pp. 509-516 ◽

Cited By ~ 22

Author(s):

C.-G. MA ◽

G.-X. ZHANG ◽

B.-G. XIAO ◽

H. LINK

Keyword(s):

Growth Factor ◽

Myasthenia Gravis ◽

Interferon Gamma ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Ifn Gamma ◽

Experimental Autoimmune Myasthenia Gravis ◽

Autoimmune Myasthenia ◽

Growth Factor Beta ◽

Experimental Autoimmune

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Interleukin-2 (IL-2) Augments the Expression of Transforming Growth Factor Beta in Patients with Disseminated Cancer

Growth Factors, Peptides and Receptors ◽

10.1007/978-1-4615-2846-3_41 ◽

1993 ◽

pp. 425-433 ◽

Cited By ~ 1

Author(s):

Pauli Puolakkainen ◽

Paolo Alberto Paciucci ◽

Jane E. Ranchalis ◽

Leslie Oleksowicz ◽

Daniel R. Twardzik

Keyword(s):

Growth Factor ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Interleukin 2 ◽

Growth Factor Beta

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Analysis of transforming growth factor-beta 1 (TGF-β1) expression in human monocytes infected with Mycobacterium avium at a single cell level by ELISPOT assay

Journal of Immunological Methods ◽

10.1016/s0022-1759(01)00485-9 ◽

2002 ◽

Vol 259 (1-2) ◽

pp. 25-32 ◽

Cited By ~ 14

Author(s):

Htin Aung ◽

Julie Sherman ◽

Magdalena Tary-Lehman ◽

Zahra Toossi

Keyword(s):

Growth Factor ◽

Mycobacterium Avium ◽

Transforming Growth Factor Beta ◽

Elispot Assay ◽

Transforming Growth Factor ◽

Single Cell Level ◽

Human Monocytes ◽

Cell Level ◽

Growth Factor Beta ◽

Tgf Β1

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Modulation of complement biosynthesis in human monocytes by transforming growth factor-beta (TGF-$beta;) and lipopolysaccharide

Molecular Immunology ◽

10.1016/0161-5890(93)90226-2 ◽

1993 ◽

Vol 30 ◽

pp. 17

Author(s):

HOGAN

Keyword(s):

Growth Factor ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Human Monocytes ◽

Tgf Beta ◽

Growth Factor Beta

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Expression of interferon-gamma (IFN-δ), IL-10, IL-12 and transforming growth factor-beta (TGF-β) mRNA in synovial fluid cells from patients in the early and late phases of rheumatoid arthritis (RA)

Clinical & Experimental Immunology ◽

10.1111/j.1365-2249.1996.tb08288.x ◽

2007 ◽

Vol 103 (3) ◽

pp. 357-367 ◽

Cited By ~ 86

Author(s):

A. BUCHT ◽

P. LARSSON ◽

L. WEISBROT ◽

C. THORNE ◽

P. PISA ◽

...

Keyword(s):

Rheumatoid Arthritis ◽

Growth Factor ◽

Synovial Fluid ◽

Interferon Gamma ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Growth Factor Beta ◽

Synovial Fluid Cells

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Regulation of Trypanosoma cruzi infections in vitro and in vivo by transforming growth factor beta (TGF-beta).

Journal of Experimental Medicine ◽

10.1084/jem.174.3.539 ◽

1991 ◽

Vol 174 (3) ◽

pp. 539-545 ◽

Cited By ~ 181

Author(s):

J S Silva ◽

D R Twardzik ◽

S G Reed

Keyword(s):

Growth Factor ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Tgf Beta ◽

Ifn Gamma ◽

Human Macrophages ◽

Growth Factor Beta ◽

Cruzi Infection

The effects of transforming growth factor beta (TGF-beta) on interferon gamma-mediated killing of the intracellular protozoan parasite Trypanosoma cruzi and on the course of T. cruzi infection in mice were investigated. Spleen cells from mice with acute T. cruzi infections were found to produce elevated levels of biologically active TGF-beta in vitro, and the possibility that TGF-beta may mediate certain aspects of T. cruzi infection was then addressed. When mouse peritoneal macrophages were treated with TGF-beta in vitro, the ability of IFN-gamma to activate intracellular inhibition of the parasite was blocked. This occurred whether cells were treated with TGF-beta either before or after IFN-gamma treatment. TGF-beta treatment also blocked the T. cruzi-inhibiting effects of IGN-gamma on human macrophages. Additionally, treatment of human macrophages with TGF-beta alone led to increased parasite replication in these cells. The effects of TGF-beta on T. cruzi infection in vivo were then investigated. Susceptible C57BL/6 mice developed higher parasitemias and died earlier when treated with TGF-beta during the course of infection. Resistant C57BL/6 x DBA/2 F1 mice treated with TGF-beta also had increased parasitemias, and 50% mortality, compared with no mortality in infected, saline-treated controls. A single dose of TGF-beta, given at the time of infection, was sufficient to significantly decrease resistance to infection in F1 mice and to exacerbate infection in susceptible C57BL/6 mice. Furthermore, a single injection of TGF-beta was sufficient to counter the in vivo protective effects of IFN-gamma. We conclude that TGF-beta, produced during acute T. cruzi infection in mice, is a potent inhibitor of the effects of macrophage activating cytokines in vivo and in vitro and may play a role in regulating infection.

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