Demonstration of immunoreactive vasoactive intestinal peptide (IR-VIP) and somatostatin (IR-SOM) in rat thymus

Gomariz, Rosa P.; Lorenzo, María Jesús López; Cacicedo, Lucinda; Vicente, Ángeles; Zapata, A.

doi:10.1016/0889-1591(90)90017-k

Cited by 68 publications

(33 citation statements)

References 25 publications

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“…The highest concentration of these SST-producing cells is in the thymic medulla and at the cortical-medullary junction (unpublished observations). Our data support the previous observations associating SST with murine thymic dendritic cells (19) and rat thymus (20,21).…”

Section: Role Of Sst In the Murine Thymussupporting

confidence: 83%

The somatostatin immunoregulatory circuit present at sites of chronic inflammation

Weinstock

Elliott²

2000

European Journal of Endocrinology

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Somatostatin is part of an immunoregulatory circuit that helps limit interferon-g (IFNg) production at sites of chronic in¯ammation. In murine schistosomiasis, parasite eggs induce focal, chronic granulomatous in¯ammation in the liver and intestines. These granulomas produce somatostatin 1±14 and express somatostatin receptor subtype number 2 (SSTR 2 ), which is the exclusive somatostatin receptor present in this in¯ammation. Granuloma and splenic macrophages as well as macrophage cell lines make somatostatin. There appears to be no other in¯ammatory cell source of the peptide. Various in¯ammatory mediators induce this expression, whereas substance P inhibits somatostatin production. Somatostatin can suppress IFNg secretion from T cells via interaction with the SSTR 2 receptor expressed on these cells. Other cells within the granuloma also display SSTR 2 . The effect of somatostatin on these other cell types remains unknown. The thymus of normal mice has a complete somatostatin regulatory circuit. The thymic epithelial and dendritic cells make somatostatin. Like the granulomas of murine schistosomiasis, the thymus expresses only SSTR 2 . Somatostatin likely has an important role in thymic T cell education and selection.

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Section: Role Of Sst In the Murine Thymussupporting

confidence: 83%

The somatostatin immunoregulatory circuit present at sites of chronic inflammation

Weinstock

Elliott²

2000

European Journal of Endocrinology

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“…7), it may be that multiple copies of the CRE can produce an effect of CREB as observed by Meinkoth et al Distinct regulation of the somatostatin and VIP promoters is expected in light of the fact that somatostatin and VIP are known to be physiologically antagonistic (36,48) and expressed in different cell types (16,30). Further characterization of the requirements for CRE function in F9 cells may therefore enable insight into the factors that allow appropriate expression of somatostatin and VIP.…”

Section: Resultsmentioning

confidence: 99%

Cyclic AMP response element-binding protein and the catalytic subunit of protein kinase A are present in F9 embryonal carcinoma cells but are unable to activate the somatostatin promoter.

Masson¹,

Ellis²,

Goodbourn³

et al. 1992

Mol. Cell. Biol.

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The cyclic AMP (cAMP) response elements (CREs) of the somatostatin and vasoactive intestinal peptide (VIP) promoters contain binding sites for CRE-binding protein (CREB) that are essential for cAMP-regulated transcription. Using F9 embryonal carcinoma cells, we show that the somatostatin and VIP promoters exhibit a differentiation-dependent cAMP response, demonstrating that these promoters are regulated by transcription factors that become active during differentiation. Lack of cAMP responsiveness of the somatostatin promoter in undifferentiated cells is not due to the absence of known positive-acting factors (the catalytic subunit of protein kinase A [cPKAJ and CREB) or a general inhibition of protein kinase A activity. Since overexpression of exogenous cPKA and CREB is sufficient to activate the somatostatin promoter in undifferentiated cells, these findings suggest that a negative factor(s) represses endogenous cPKA and CREB. In contrast to their effects on somatostatin, exogenous CREB and cPKA do not activate the VIP promoter. Thus, despite coregulation during differentiation and the ability to bind CREB, the somatostatin and VIP promoters are not coordinately activated by CREB in undifferentiated F9 cells.

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“…3). The first evidence was the presence of VIP-ir in thymus, spleen, and lymph node cells using immunohistological methods (Gomariz et al, 1990(Gomariz et al, , 1992, where most VIP-ir was strongly identified in cells with lymphocyte appearance. VIP ϩ lymphocytes are more numerous in the thymic deep cortex and medulla, in the splenic periarteriolar lymphoid sheaths, and in the lymph node T cell-dependent interfollicular areas and deep cortex.…”

Section: Vasoactive Intestinal Peptide Production By Mastmentioning

confidence: 99%

The Significance of Vasoactive Intestinal Peptide in Immunomodulation

Delgado

Pozo²,

Ganea³

2004

Pharmacol Rev

370

319

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Demonstration of immunoreactive vasoactive intestinal peptide (IR-VIP) and somatostatin (IR-SOM) in rat thymus

Cited by 68 publications

References 25 publications

The somatostatin immunoregulatory circuit present at sites of chronic inflammation

The somatostatin immunoregulatory circuit present at sites of chronic inflammation

Cyclic AMP response element-binding protein and the catalytic subunit of protein kinase A are present in F9 embryonal carcinoma cells but are unable to activate the somatostatin promoter.

The Significance of Vasoactive Intestinal Peptide in Immunomodulation

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