Interferon regulatory factor-1 is inducible by prolactin, interleukin-2 and concanavalin A in T cells

Schwarz, Lindsay A.; Stevens, Anne M.; Hrachovy, Julie A.; Yu-Lee, Li-yuan

doi:10.1016/0303-7207(92)90180-e

Cited by 39 publications

(18 citation statements)

References 26 publications

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“…The rat Nb2 T lymphoma cell line (13) has been used extensively as a model system to study the molecular mechanisms underlying PRL signaling in T cells (14). Previous studies from our laboratory have found that PRL induces the expression of a number of early growth-related genes including interferon regulatory factor 1 (IRF-1) as part of an early activation program leading to mitogenesis (15)(16)(17). Our studies have identified the interferon-␥ activation sequence (GAS) in the IRF-1 promoter as a PRL-responsive enhancer element (18 -20).…”

mentioning

confidence: 95%

Transcriptional Inhibition by Stat5

Luo

Yu-Lee

1997

Journal of Biological Chemistry

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Signal transduction through the cytokine/hematopoietin receptor superfamily involves the activation of the Janus kinase (JAK) 1 /signal transducer and activator of transcription (Stat) pathway (1-3). Cytokine binding to its receptor rapidly activates JAK tyrosine kinases, which are either prebound or recruited to the receptor upon tyrosine phosphorylation. Activated JAK tyrosine kinases then phosphorylate the receptor itself and Stats that are recruited to the receptor through the interaction between the Src homology (SH2) domain on the Stats and phosphorylated tyrosine residues on the receptor. Phosphorylated Stats form homo-or heteromeric complexes, translocate into the nucleus, bind to specific DNA elements, and participate in target gene transcription.

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confidence: 95%

Transcriptional Inhibition by Stat5

Luo

Yu-Lee

1997

Journal of Biological Chemistry

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“…STAT5 has been shown to be activated by PRL in mammary epithelial cells, and both PRL and IL-2 induce transcription of the IRF-1 gene in T lymphocytes (4,5,15). For these reasons we determined whether STAT5 is activated in Nb2 T cells in response to stimulation by PRL or IL-2.…”

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confidence: 99%

“…IL-2 and PRL are cytokines responsible for inducing distinct physiological responses, yet they both stimulate T-lymphocyte proliferation and differentiation (14)(15)(16)(17)(18)(19)(20)(21). IL-2, produced by T lymphocytes, binds to a transmembrane receptor composed of three subunits (a, B, and 'y chains) that oligomerize after ligand binding (20)(21)(22).…”

mentioning

confidence: 99%

Interleukin 2 activates STAT5 transcription factor (mammary gland factor) and specific gene expression in T lymphocytes.

Gilmour

Pine²,

Reich³

1995

Proc. Natl. Acad. Sci. U.S.A.

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Although prolactin and interleukin 2 (IL-2) can elicit distinct physiological responses, we have found that their signal pathways share a common signal transducer and activator of transcription, STAT5. STAT5 was originally identified as a mammary gland factor induced by prolactin in lactating breast cells. Here we demonstrate that STAT5 is activated after IL-2 stimulation of two responsive lymphocyte cell lines, Nb2 and YT. Activation of STAT5 is measured both by IL-2-induced tyrosine phosphorylation and by IL-2-induced DNA binding. The STAT5 DNA recognition site is the same as the interferon y-activated site (GAS) in the interferon regulatory factor 1 gene. We demonstrate that the GAS element is necessary and sufficient for transcriptional induction by both IL-2 and prolactin in T lymphocytes. These results indicate that the role of STAT5 in the regulation of gene expression is not restricted to mammary cells or to prolactin, but is an integral part of the signal pathway of a critical immunomodulatory cytokine, IL-2.Recent advances in the field of cytokine research have identified signal transduction pathways that initiate at a cell surface receptor and culminate in the activation of specific gene expression in the nucleus. Such a receptor-to-nucleus signal pathway was originally demonstrated in the interferon system and involves the activation of tyrosine kinases of the Janus kinase (JAK) family that phosphorylate latent cytoplasmic transcription factors called signal transducers and activators of transcription (STATs) (reviewed in refs.

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“…The abundance of prolactin receptors therein suggests that prolactin might be able to modulate the atherosclerotic process. Prolactin is widely accepted as an important physiological modulator of the immune response (Pellegrini et al 1992, Schwarz et al 1992, Dorshkind & Horseman 2000. In addition, atherosclerosis is now recognized as a chronic low-grade inflammatory condition of the vessel wall, characterized by infiltration of macrophages and T-cells, which interact with one another and with other cells of the arterial wall (Packard & Libby 2008).…”

Section: Discussionmentioning

confidence: 99%

“…In fact, prolactin is widely recognized as an important physiological modulator of the immune response (Dorshkind & Horseman 2000). For instance, prolactin stimulates T-cell proliferation (Clevenger et al 1990), and it supports interferon-g production (Schwarz et al 1992). Furthermore, prolactin has been shown to be involved in regulating monocyte/macrophage function in vitro (Aziz et al 2008, Carvalho-Freitas et al 2008.…”

Section: Introductionmentioning

confidence: 99%

The prolactin receptor is expressed in macrophages within human carotid atherosclerotic plaques: a role for prolactin in atherogenesis?

Reuwer¹,

Eijk²,

Houttuijn-Bloemendaal³

et al. 2010

Journal of Endocrinology

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Atherosclerotic vascular disease is the consequence of a chronic inflammatory process, and prolactin has been shown to be a component of the inflammatory response. Additionally, recent studies indicate that prolactin contributes to an atherogenic phenotype. We hypothesized that this may be the result of a direct effect of prolactin on atherogenesis through activation of the prolactin receptor. Human carotid atherosclerotic plaques were obtained from patients by endarteriectomies. The mRNA of prolactin receptor, but not of prolactin, was detected in these atherosclerotic plaques by quantitative realtime PCR. In situ hybridization confirmed the expression of the prolactin receptor in mononuclear cells. Analysis at the protein level using immunohistochemistry and immunoelectron microscopy revealed that the prolactin receptor was abundantly present in macrophages near the lipid core and shoulder regions of the plaques. Our findings demonstrate that the prolactin receptor is present in macrophages of the atherosclerotic plaque at sites of most prominent inflammation. We therefore propose that prolactin receptor signaling contributes to the local inflammatory response within the atherosclerotic plaque and thus to atherogenesis.

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Interferon regulatory factor-1 is inducible by prolactin, interleukin-2 and concanavalin A in T cells

Cited by 39 publications

References 26 publications

Transcriptional Inhibition by Stat5

Transcriptional Inhibition by Stat5

Interleukin 2 activates STAT5 transcription factor (mammary gland factor) and specific gene expression in T lymphocytes.

The prolactin receptor is expressed in macrophages within human carotid atherosclerotic plaques: a role for prolactin in atherogenesis?

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