VIP and tolerance induction in autoimmunity

Vasoactive intestinal peptide (VIP) is a potent antiinflammatory agent with immunoregulatory properties, skewing the immune response to a Th2 pattern of cytokine production. Here, we studied the effect of treatment with VIP in the development of diabetes in nonobese diabetic (NOD) mice, an annual mo...

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Autores principales: Rosignoli, F., Torroba, M., Juarranz, Y., García-Gómez, M., Martinez, C., Gomariz, R.P., Pérez-Leirós, C., Leceta, J.
Formato: SER
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VIP
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_00778923_v1070_n_p525_Rosignoli
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spelling todo:paper_00778923_v1070_n_p525_Rosignoli2023-10-03T14:54:17Z VIP and tolerance induction in autoimmunity Rosignoli, F. Torroba, M. Juarranz, Y. García-Gómez, M. Martinez, C. Gomariz, R.P. Pérez-Leirós, C. Leceta, J. Autoimmune FoxP3 TGF-β VIP cytokine transcription factor transcription factor T bet transforming growth factor beta vasoactive intestinal polypeptide animal experiment animal model autoimmunity cell differentiation cell function conference paper controlled study down regulation drug mechanism female insulin dependent diabetes mellitus insulitis mouse nonhuman pancreas pancreas islet regulatory T lymphocyte Th1 cell upregulation Animalia Vasoactive intestinal peptide (VIP) is a potent antiinflammatory agent with immunoregulatory properties, skewing the immune response to a Th2 pattern of cytokine production. Here, we studied the effect of treatment with VIP in the development of diabetes in nonobese diabetic (NOD) mice, an annual model of type 1 diabetes. Mice treated with VIP from 4 weeks of age did not develop diabetes and showed milder insulitis than nontreated mice. The protective mechanism of VIP was associated with a reduction in the circulating levels of Th1 cytokines. In the pancreas of VIP-treated animals, regulatory T cell markers predominate, as indicated by the upregulation of FoxP3 and transforming growth factor-β (TGF-β), and the downregulation of the transcription factor, T-bet. These findings indicate that VIP restores tolerance to pancreatic islets by promoting the local differentiation and function of regulatory T cells. © 2006 New York Academy of Sciences. Fil:Rosignoli, F. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Pérez-Leirós, C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. SER info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_00778923_v1070_n_p525_Rosignoli
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Autoimmune
FoxP3
TGF-β
VIP
cytokine
transcription factor
transcription factor T bet
transforming growth factor beta
vasoactive intestinal polypeptide
animal experiment
animal model
autoimmunity
cell differentiation
cell function
conference paper
controlled study
down regulation
drug mechanism
female
insulin dependent diabetes mellitus
insulitis
mouse
nonhuman
pancreas
pancreas islet
regulatory T lymphocyte
Th1 cell
upregulation
Animalia
spellingShingle Autoimmune
FoxP3
TGF-β
VIP
cytokine
transcription factor
transcription factor T bet
transforming growth factor beta
vasoactive intestinal polypeptide
animal experiment
animal model
autoimmunity
cell differentiation
cell function
conference paper
controlled study
down regulation
drug mechanism
female
insulin dependent diabetes mellitus
insulitis
mouse
nonhuman
pancreas
pancreas islet
regulatory T lymphocyte
Th1 cell
upregulation
Animalia
Rosignoli, F.
Torroba, M.
Juarranz, Y.
García-Gómez, M.
Martinez, C.
Gomariz, R.P.
Pérez-Leirós, C.
Leceta, J.
VIP and tolerance induction in autoimmunity
topic_facet Autoimmune
FoxP3
TGF-β
VIP
cytokine
transcription factor
transcription factor T bet
transforming growth factor beta
vasoactive intestinal polypeptide
animal experiment
animal model
autoimmunity
cell differentiation
cell function
conference paper
controlled study
down regulation
drug mechanism
female
insulin dependent diabetes mellitus
insulitis
mouse
nonhuman
pancreas
pancreas islet
regulatory T lymphocyte
Th1 cell
upregulation
Animalia
description Vasoactive intestinal peptide (VIP) is a potent antiinflammatory agent with immunoregulatory properties, skewing the immune response to a Th2 pattern of cytokine production. Here, we studied the effect of treatment with VIP in the development of diabetes in nonobese diabetic (NOD) mice, an annual model of type 1 diabetes. Mice treated with VIP from 4 weeks of age did not develop diabetes and showed milder insulitis than nontreated mice. The protective mechanism of VIP was associated with a reduction in the circulating levels of Th1 cytokines. In the pancreas of VIP-treated animals, regulatory T cell markers predominate, as indicated by the upregulation of FoxP3 and transforming growth factor-β (TGF-β), and the downregulation of the transcription factor, T-bet. These findings indicate that VIP restores tolerance to pancreatic islets by promoting the local differentiation and function of regulatory T cells. © 2006 New York Academy of Sciences.
format SER
author Rosignoli, F.
Torroba, M.
Juarranz, Y.
García-Gómez, M.
Martinez, C.
Gomariz, R.P.
Pérez-Leirós, C.
Leceta, J.
author_facet Rosignoli, F.
Torroba, M.
Juarranz, Y.
García-Gómez, M.
Martinez, C.
Gomariz, R.P.
Pérez-Leirós, C.
Leceta, J.
author_sort Rosignoli, F.
title VIP and tolerance induction in autoimmunity
title_short VIP and tolerance induction in autoimmunity
title_full VIP and tolerance induction in autoimmunity
title_fullStr VIP and tolerance induction in autoimmunity
title_full_unstemmed VIP and tolerance induction in autoimmunity
title_sort vip and tolerance induction in autoimmunity
url http://hdl.handle.net/20.500.12110/paper_00778923_v1070_n_p525_Rosignoli
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AT torrobam vipandtoleranceinductioninautoimmunity
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AT garciagomezm vipandtoleranceinductioninautoimmunity
AT martinezc vipandtoleranceinductioninautoimmunity
AT gomarizrp vipandtoleranceinductioninautoimmunity
AT perezleirosc vipandtoleranceinductioninautoimmunity
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