Inhibitory effect of somatostatin on human T lymphocytes proliferation

Casnici, Claudia; Lattuada, D.; Perego, Carla; Franco, Paola; Marelli, O

doi:10.1016/s0192-0561(97)00033-7

Cited by 29 publications

(23 citation statements)

References 19 publications

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“…Most of these studies involved mixed cell populations under T cell-stimulating conditions. The most significant inhibitory effects of SRIF are observed when purified T lymphocytes or T cell lines are used under suboptimal stimulation conditions (Casnici et al, 1997;Krco et al, 1986;Payan et al, 1984). The use of strong activating lectins or cytokines may overrule the effect of a sst agonist or antagonist.…”

Section: Effect Of Srif On the T Cell Lineagementioning

confidence: 99%

The role of cortistatin in the human immune system

Hagen

Dalm

Staal

et al. 2008

Molecular and Cellular Endocrinology

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Please cite this article as: van Hagen, P.M., Dalm, V.A., Staal, F., Hofland, L.J., The Role of Cortistatin in the Human Immune System, Molecular and Cellular Endocrinology (2007Endocrinology ( ), doi:10.1016Endocrinology ( /j.mce.2008 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. AbstractCortistatin (CST) is a recently described neuropeptide that shares high homology with somatostatin (somatotropin release-inhibiting factor, SRIF) and binds with high affinity to all somatostatin receptor (sst) subtypes. CST is currently known to have a widespread distribution in many human organs including the immune system. The activities specific to CST may be partially attributable to its binding to the growth hormone secretagogue (GHS) receptor (GHS-R) and the orphan Gprotein-coupled receptor MrgX2. Human immune cells produce CST, whereas macrophage lineage and activated endothelium express sst 2 , and human lymphocytes express sst 3 . The human thymus expresses sst 1,2,3 , MrgX2 and almost all immune cells express GHS-R. Moreover, at this very moment promising research with CST in experimental animal models is being performed. On the basis of these promising results, studies aiming to further evaluate the possibilities of CST as a therapeutic agent in human immune mediated inflammatory diseases are warranted.

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Section: Effect Of Srif On the T Cell Lineagementioning

confidence: 99%

The role of cortistatin in the human immune system

Hagen

Dalm

Staal

et al. 2008

Molecular and Cellular Endocrinology

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“…SOM inhibits IFN-Á production by staphylococcal enterotoxin-A-stimulated human peripheral blood mononuclear cells [23] and in schistosome granulomas [24], and also inhibits the release of IL-6 from LPS-activated human peripheral blood monocytes cultured in vitro [25,26]. These suppressive effects of SOM on cytokine production may be coupled with the known inhibitiory effects of SOM on lymphocyte proliferation [27]. SP enhances IFN-Á production by pokeweed mitogen-stimulated peripheral blood mononuclear cells [28] and in schistosome granulomas [24], and also induces the sysnthesis of IL-6 in human peripheral blood mononuclear cells [13,29].…”

Section: Discussionmentioning

confidence: 94%

Somatostatin and Substance P Induced in vivo by Lipopolysaccharide and in Peritoneal Macrophages Stimulated with Lipopolysaccharide or Interferon-Gamma Have Differential Effects on Murine Cytokine Production

Ryu

Jeong²,

Yoon³

et al. 2000

Neuroimmunomodulation

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We have investigated whether lipopolysaccharide (LPS) induces substance P (SP) and somatostatin (SOM) in popliteal lymph nodes in vivo and whether macrophages are a source of SP and SOM in vitro. We have also investigated the effect of SP and SOM treatment on the production of cytokines. SP reached a maximum 3 days after injection of LPS (100 μg/footpad) and then declined. SOM expression after LPS injection reached a maximum at 5–7 days. Stimulation of thioglycolate-elicited peritoneal macrophages with LPS (20 μg/ml), recombinant interferon-γ (rIFN-γ, 100 U/ml), and LPS plus rIFN-γ induced SOM and SP. Thioglycolate-elicited, unstimulated peritoneal macrophages also synthesized these peptides. SOM (10^–12–10^–8 M) significantly inhibited IL-6 and IFN-γ production, whereas SP at those concentrations enhanced cytokine production by activated lymphocytes and macrophages. These findings suggest that neuropeptides which originate from macrophages and nerve fibers act as immunomodulators to mediate changes in the pattern of cytokine production.

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“…On the other hand, sst 3 is involved in apoptosis by inducing p53 and BAX (Sharma et al, 1996;Sharma and Srikant, 1998). In recent years both inhibitory (Atiya et al, 1997;Casnici et al, 1997;Lattuada et al, 2007;Payan et al, 1984) and stimulatory (Johansson and Sandberg, 1989; Krantic et al, 1997) effects of SS or its analogues on cell proliferation have been described.…”

Section: Cell Proliferationmentioning

confidence: 99%