Transforming growth factor–β and Notch ligands act as opposing environmental cues in regulating the plasticity of type 3 innate lymphoid cells

2016 ◽  
Vol 9 (426) ◽  
pp. ra46-ra46 ◽  
Author(s):  
Charlotte Viant ◽  
Lucille C. Rankin ◽  
Mathilde J. H. Girard-Madoux ◽  
Cyril Seillet ◽  
Wei Shi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Environmental Cues ◽  
Type 3 ◽  
Notch Ligands

scholarly journals Transforming Growth Factor-β Signaling Guides the Differentiation of Innate Lymphoid Cells in Salivary Glands

Immunity ◽  
2016 ◽  
Vol 44 (5) ◽  
pp. 1127-1139 ◽  
Author(s):  
Victor S. Cortez ◽  
Luisa Cervantes-Barragan ◽  
Michelle L. Robinette ◽  
Jennifer K. Bando ◽  
Yaming Wang ◽  
...  
Keyword(s):  
Growth Factor ◽  
Salivary Glands ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells

scholarly journals Requirement for the SnoN Oncoprotein in Transforming Growth Factor β-Induced Oncogenic Transformation of Fibroblast Cells

2005 ◽  
Vol 25 (24) ◽  
pp. 10731-10744 ◽  
Author(s):  
Qingwei Zhu ◽  
Sonia Pearson-White ◽  
Kunxin Luo
Keyword(s):  
Growth Factor ◽  
Epithelial Cells ◽  
Cancer Cells ◽  
Transforming Growth Factor ◽  
Human Cancer ◽  
Transforming Growth Factor Β ◽  
Lymphoid Cells ◽  
Human Cancer Cells ◽  
Inhibitory Site ◽  
Transforming Activity

ABSTRACT Transforming growth factor β (TGF-β) was originally identified by virtue of its ability to induce transformation of the AKR-2B and NRK fibroblasts but was later found to be a potent inhibitor of the growth of epithelial, endothelial, and lymphoid cells. Although the growth-inhibitory pathway of TGF-β mediated by the Smad proteins is well studied, the signaling pathway leading to the transforming activity of TGF-β in fibroblasts is not well understood. Here we show that SnoN, a member of the Ski family of oncoproteins, is required for TGF-β-induced proliferation and transformation of AKR-2B and NRK fibroblasts. TGF-β induces upregulation of snoN expression in both epithelial cells and fibroblasts through a common Smad-dependent mechanism. However, a strong and prolonged activation of snoN transcription that lasts for 8 to 24 h is detected only in these two fibroblast lines. This prolonged induction is mediated by Smad2 and appears to play an important role in the transformation of both AKR-2B and NRK cells. Reduction of snoN expression by small interfering RNA or shortening of the duration of snoN induction by a pharmacological inhibitor impaired TGF-β-induced anchorage-independent growth of AKR-2B cells. Interestingly, Smad2 and Smad3 play opposite roles in regulating snoN expression in both fibroblasts and epithelial cells. The Smad2/Smad4 complex activates snoN transcription by direct binding to the TGF-β-responsive element in the snoN promoter, while the Smad3/Smad4 complex inhibits it through a novel Smad inhibitory site. Mutations of Smad4 that render it defective in heterodimerization with Smad3, which are found in many human cancers, convert the activity of Smad3 on the snoN promoter from inhibitory to stimulatory, resulting in increased snoN expression in cancer cells. Thus, we demonstrate a novel role of SnoN in the transforming activity of TGF-β in fibroblasts and also uncovered a mechanism for the elevated SnoN expression in some human cancer cells.

scholarly journals 1022: Transforming Growth Factor β Type 3 Receptor is a Tumor Suppressor Gene in Conventional Renal Cell Carcinoma

2004 ◽  
Vol 171 (4S) ◽  
pp. 270-270
Author(s):  
John A. Copland ◽  
Tapaty Maity ◽  
Shauna LeGrand ◽  
Pheroze Tamboli ◽  
Joanna Taormina ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Growth Factor ◽  
Tumor Suppressor ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Suppressor Gene ◽  
Conventional Renal Cell Carcinoma ◽  
Type 3

scholarly journals Transforming Growth Factor-β Promotes Inactivation of Extracellular Thyroid Hormones via Transcriptional Stimulation of Type 3 Iodothyronine Deiodinase

2005 ◽  
Vol 19 (12) ◽  
pp. 3126-3136 ◽  
Author(s):  
Stephen A. Huang ◽  
Michelle A. Mulcahey ◽  
Alessandra Crescenzi ◽  
Mirra Chung ◽  
Brian W. Kim ◽  
...  
Keyword(s):  
Growth Factor ◽  
Thyroid Hormones ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Iodothyronine Deiodinase ◽  
Type 3 ◽  
Stimulation Of ◽  
Transcriptional Stimulation

scholarly journals Possible role of transforming growth factor β as a marker cytokine of type 3 T-helpers in atopic dermatitis pathogenesis

2004 ◽  
Vol 3 (3) ◽  
pp. 27-31
Author(s):  
N. A. Pronina ◽  
V. S. Sviridova ◽  
A. A. Denisov ◽  
V. V. Klimov ◽  
Ye. N. Kologrivova
Keyword(s):  
Atopic Dermatitis ◽  
Biological Activity ◽  
Growth Factor ◽  
Molecular Mechanisms ◽  
Transforming Growth Factor ◽  
Allergic Inflammation ◽  
Transforming Growth Factor Β ◽  
Cell Populations ◽  
Type 3

The role of transforming growth factor β (TGF-β) in atopic dermatitis pathogenesis is discussed basing on the analysis of existing data of cellular and molecular mechanisms of allergic inflammation. Up-to date data of the main T-helper (T-h) lymphocyte subpopulations including Tx1, Tx2, Tx3 has been presented. Functions of regulatory T-cell populations and produced cytokines have been described. The main attention has been accented on the TGF-β structure and biological activity as a main Tx3 cytokine. The current information of TGF-β influence on different cell populations and its biological activity realization mechanism is thoroughly discussed. Information relating to the mechanism of cytokine regulation during atopic dermatitis has been summarized. A deep analysis of possible participation of TGF-β in disbalance formation on Tx1 and Tx2 levels, in disturbances of histological derma structure and allergic inflammation timing has been made.

Perianale Fisteln bei CED: vom Mausmodell zur Klinik

2018 ◽  
Vol 75 (5) ◽  
pp. 287-294
Author(s):  
Michael Scharl
Keyword(s):  
Growth Factor ◽  
Morbus Crohn ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Interleukin 13

Zusammenfassung. Fisteln stellen nach wie vor eine der wichtigsten Komplikationen bei Patienten mit Morbus Crohn dar. Bei mindestens einem Drittel aller Morbus Crohn Patienten treten im Laufe der Erkrankung Fisteln auf. Eine dauerhafte Heilung der Fistel wird jedoch, auch unter Ausschöpfung sämtlicher medikamentöser und chirurgischer Therapieoptionen, nur in rund einem Drittel dieser Patienten erreicht. Der genaue molekulare Mechanismus der Fistelentstehung ist bis heute nicht ganz klar. Aus histopathologischer Sichtweise stellen Fisteln eine röhrenartige Struktur dar, welche von flachen epithelartigen Zellen ausgekleidet ist. Als ursächlicher Entstehungsmechanismus wird dabei die sogenannte epitheliale-zu-mesenchymale Transition (EMT) angesehen und es kann eine starke Expression der Entzündungsmediatoren Tumor Nekrose Faktor, Interleukin-13 und Transforming Growth Factor β in den Fistelarealen nachgewiesen werden. Zusätzlich zu den bereits etablierten, medikamentösen Therapieoptionen, also Antibiotika, Immunmodulatoren und anti-TNF Antikörper, stellt insbesondere der Einsatz der mesenchymalen Stammzelltherapie einen erfolgversprechenden Therapieansatz für die Zukunft dar.

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