Biologic functions of the IFN‐γ receptors

Tau, Gregory; Rothman, Paul B.

doi:10.1034/j.1398-9995.1999.00099.x

Cited by 221 publications

(171 citation statements)

References 220 publications

(235 reference statements)

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“…1E). Together, these data suggest that CD8 ϩ T cells are unable to respond to IFN-␥ because they may lack IFN-␥R2, the signal-transducing component of the IFN-␥R (38).…”

Section: Cd8 ϩ T Cells Do Not Express Ifn-␥r2 Mrna and Are Unresponsimentioning

confidence: 93%

Regulation of IFN-γ Signaling Is Essential for the Cytotoxic Activity of CD8+ T Cells

Tau¹,

Cowan²,

Weisburg³

et al. 2001

The Journal of Immunology

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Previous studies have demonstrated that, as naive murine CD4+ cells differentiate into Th1 cells, they lose expression of the second chain of IFN-γR (IFN-γR2). Hence, the IFN-γ-producing subset of Th cells is unresponsive to IFN-γ. Analysis of IFN-γ-producing CD8+ T cells demonstrates that, like Th1 cells, these cells do not express IFN-γR2. To define the importance of IFN-γ signaling for the development of functional CD8+ T cells, mice either lacking IFN-γR2 or overexpressing this protein were examined. While CD8+ T cell development and function appear normal in IFN-γR2−/− mice, CD8+ T cell function in IFN-γR2 transgenic is altered. IFN-γR2 transgenic CD8+ T cells are unable to lyse target cells in vitro. However, these cells produce Fas ligand, perforin, and granzyme B, the effector molecules required for killing. Interestingly, TG CD8+ T cells proliferate normally and produce cytokines, such as IFN-γ in response to antigenic stimulation. Therefore, although IFN-γ signaling is not required for the generation of normal cytotoxic T cells, constitutive IFN-γ signaling can selectively impair the cytotoxic function of CD8+ T cells.

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“…1E). Together, these data suggest that CD8 ϩ T cells are unable to respond to IFN-␥ because they may lack IFN-␥R2, the signal-transducing component of the IFN-␥R (38).…”

Section: Cd8 ϩ T Cells Do Not Express Ifn-␥r2 Mrna and Are Unresponsimentioning

confidence: 93%

Regulation of IFN-γ Signaling Is Essential for the Cytotoxic Activity of CD8+ T Cells

Tau¹,

Cowan²,

Weisburg³

et al. 2001

The Journal of Immunology

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show abstract

“…The broad effects of IFN-␥ include activation of macrophages and antiviral immunity, enhancement of Ag presentation and induction of MHC-peptide complexes, orchestration of lymphocyte-endothelial interactions, regulation of T cell polarization toward T H 1/T H 2, cellular proliferation, and stimulation of apoptosis (3). The obvious importance in cellular immunity of these diverse IFN-␥-mediated actions is highlighted in the observation that humans and mice with IFN-␥R deficiency show a marked susceptibility to intracellular bacterial and several viral infections (2,4).…”

Section: Role Of Direct Effects Of Ifn-␥ On T Cells In the Regulationmentioning

confidence: 99%

“…The cellular effects of IFN-␥ are mediated by its heterodimeric cell surface receptor IFN-␥R. The IFN-␥R is comprised of ␣-and ␤-chains, both of which belong to the class II family of cytokine receptors (1,2). IFN-␥R is expressed ubiquitously on all nucleated cells, including T cells, and therefore IFN-␥ exerts distinct effects in a wide range of target cells (1,3).…”

Section: Role Of Direct Effects Of Ifn-␥ On T Cells In the Regulationmentioning

confidence: 99%

Role of Direct Effects of IFN-γ on T Cells in the Regulation of CD8 T Cell Homeostasis

Tewari

Nakayama

Suresh

2007

The Journal of Immunology

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It is well recognized that IFN-γ plays a critical role in the control of CD8 T cell expansion and contraction during immune responses to several intracellular pathogens. However, our understanding of the mechanisms underlying the regulation of T cell fate by IFN-γ is sorely incomplete. Specifically, it is unclear whether regulation of CD8 T cell homeostasis occurs by a T cell intrinsic IFN-γ pathway. In this study, we have determined the role of the direct effects of IFN-γ on T cells in regulating the expansion, contraction, and memory phases of the polyclonal CD8 T cell response to an acute viral infection. Using two complementary approaches we demonstrate that the direct effects of IFN-γ suppress IL-7R expression on Ag-specific effector CD8 T cells, but clonal expansion or deletion of activated CD8 T cells in vivo can occur in the apparent absence of IFN-γR signaling in T cells. These findings have clarified fundamental features of control of T cell homeostasis by IFN-γ in the context of CD8 T cell memory and protective immunity.

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“…The receptor complex consists of two chains: IFN-γR1 (also known as IFN-γ receptor α), which is the major ligand-binding subunit, and IFN-γR2 (also known as IFN-γ receptor β), which is obligatory for IFN-γ signal transduction, and also increases the affinity of IFN-γR1 for its ligand, presumably by enhancing the stability of the complex (Boehm et al 1997, Tau & Rothman 1999.…”

mentioning

confidence: 99%