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TGF-Beta Signaling in Chronic Inflammation and Cancer: From Immunosuppression to...
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TGF-Beta Signaling in Chronic Inflammation and Cancer: From Immunosuppression to Tissue Remodeling

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (28 February 2023) | Viewed by 7215

Special Issue Editor

Prof. Dr. Susetta Finotto

E-Mail Website1 Website2
Guest Editor
Department of Molecular Pneumology, Friedrich-Alexander-University (FAU) Erlangen-Nürnberg, Universitätsklinikum Erlangen, 91052 Erlangen, Germany
Interests: allergic asthma; immunoregulation; anti-viral immune responses; anti-tumor immune responses
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Transforming growth factor-β (TGF-β) is a pleiotropic cytokine with key regulatory roles in tissue homeostasis, inflammation and cancer. TGF-β signaling has cytostatic and apoptotic functions that help mammalian tissues to maintain homeostasis by restraining immune cell activation seen in autoimmunity and allergies. In these globally increasing conditions, the immune system damages its own tissues via specific molecular signaling events. These diseases are treated with immunosuppressive medications like corticosteroids or biological agents such as anti-cytokine antibodies. In allergic diseases, a hypersensitivity of the immune system to normally harmless substances in the environment causes the body to react to any contact with that substance. Thereby, TGF-β can induce tissue fibrosis and marked damage via tissue remodeling. In contrast to inflammatory disorders in which TGF-β may suppress inflammation, this cytokine may dampen anti-tumor immune responses in cancer. In fact, tumor cells can overproduce TGF-beta to create a local immunosuppressive environment that promotes tumor growth and metastasis.

For these reasons, there is a growing interest in understanding and therapeutically targeting TGF-β-mediated processes in cancer progression, and by contrast the need to understand the possible therapeutic role of TGF-beta in autoimmune and allergic disorders.

In this Special Issue, we wish to analyze the effect of TGF-beta-producing cells in health and disease. This Issue will help to find new avenues to improve current therapies for autoimmunity, allergies and cancer.

Prof. Dr. Susetta Finotto
Guest Editor

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Keywords

  • TGF-beta
  • inflammation
  • cancer

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Published Papers (3 papers)

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Research

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20 pages, 4956 KiB  
Article
Differential Modulation of miR-122 Transcription by TGFβ1/BMP6: Implications for Nonresolving Inflammation and Hepatocarcinogenesis
by Martha Paluschinski, Claus Kordes, Mihael Vucur, Veronika Buettner, Christoph Roderburg, Haifeng C. Xu, Prashant V. Shinte, Philipp A. Lang, Tom Luedde and Mirco Castoldi
Cells 2023, 12(15), 1955; https://doi.org/10.3390/cells12151955 - 27 Jul 2023
Cited by 3 | Viewed by 1344
Abstract
Chronic inflammation is widely recognized as a significant factor that promotes and worsens the development of malignancies, including hepatocellular carcinoma. This study aimed to explore the potential role of microRNAs in inflammation-associated nonresolving hepatocarcinogenesis. By conducting a comprehensive analysis of altered microRNAs in [...] Read more.
Chronic inflammation is widely recognized as a significant factor that promotes and worsens the development of malignancies, including hepatocellular carcinoma. This study aimed to explore the potential role of microRNAs in inflammation-associated nonresolving hepatocarcinogenesis. By conducting a comprehensive analysis of altered microRNAs in animal models with liver cancer of various etiologies, we identified miR-122 as the most significantly downregulated microRNA in the liver of animals with inflammation-associated liver cancer. Although previous research has indicated the importance of miR-122 in maintaining hepatocyte function, its specific role as either the trigger or the consequence of underlying diseases remains unclear. Through extensive analysis of animals and in vitro models, we have successfully demonstrated that miR-122 transcription is differentially regulated by the immunoregulatory cytokines, by the transforming growth factor-beta 1 (TGFβ1), and the bone morphogenetic protein-6 (BMP6). Furthermore, we presented convincing evidence directly linking reduced miR-122 transcription to inflammation and in chronic liver diseases. The results of this study strongly suggest that prolonged activation of pro-inflammatory signaling pathways, leading to disruption of cytokine-mediated regulation of miR-122, may significantly contribute to the onset and exacerbation of chronic liver disease. Full article
(This article belongs to the Special Issue TGF-Beta Signaling in Chronic Inflammation and Cancer: From Immunosuppression to Tissue Remodeling)
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11 pages, 2246 KiB  
Article
Rhinovirus Suppresses TGF-β-GARP Presentation by Peripheral NK Cells
by Susanne Krammer, Zuqin Yang, Hannah Mitländer, Janina C. Grund, Sonja Trump, Susanne Mittler, Sabine Zirlik and Susetta Finotto
Cells 2023, 12(1), 129; https://doi.org/10.3390/cells12010129 - 28 Dec 2022
Cited by 3 | Viewed by 1935
Abstract
Asthma is a chronic airway disease whose exacerbations are often triggered by rhinovirus infection. TGF-β1 induces rhinovirus replication in infected cells. Moreover, TGF-β1 is a pleiotropic mediator that is produced by many immune cells in the latent, inactive form bound to the latency-associated [...] Read more.
Asthma is a chronic airway disease whose exacerbations are often triggered by rhinovirus infection. TGF-β1 induces rhinovirus replication in infected cells. Moreover, TGF-β1 is a pleiotropic mediator that is produced by many immune cells in the latent, inactive form bound to the latency-associated peptide (LAP) and to the transmembrane protein glycoprotein A repetitions predominant (GARP). In this study we wanted to investigate the effect of rhinovirus infection on the TGF-β secretion and the downstream signaling via TGF-βRI/RII in peripheral blood mononuclear cells from control and asthmatic patients after rhinovirus infection ex vivo. Here, we found a significant upregulation of TGF-βRII in untouched PBMCs of asthmatics as well as a suppression of TGF-β release in the rhinovirus-infected PBMC condition. Moreover, consistent with an effect of TGF-β on Tregs, PBMCs infected with RV induced Tregs, and TGF-βRII directly correlated with RV1b mRNA. Finally, we found via flow cytometry that NK cells expressed less GARP surface-bound TGF-β, while cytokine-producing NKbright cells were induced. In summary, we show that rhinovirus infection inhibits TGF-β release in PBMCs, which results in the activation of both Treg and NK cells. Full article
(This article belongs to the Special Issue TGF-Beta Signaling in Chronic Inflammation and Cancer: From Immunosuppression to Tissue Remodeling)
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Review

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14 pages, 1026 KiB  
Review
TGFβ and the Tumor Microenvironment in Colorectal Cancer
by Maximilian J. Waldner and Markus F. Neurath
Cells 2023, 12(8), 1139; https://doi.org/10.3390/cells12081139 - 12 Apr 2023
Cited by 5 | Viewed by 2960
Abstract
Growing evidence supports an important role of the tumor microenvironment (TME) in the pathogenesis of colorectal cancer (CRC). Resident cells such as fibroblasts or immune cells infiltrating into the TME maintain continuous crosstalk with cancer cells and thereby regulate CRC progression. One of [...] Read more.
Growing evidence supports an important role of the tumor microenvironment (TME) in the pathogenesis of colorectal cancer (CRC). Resident cells such as fibroblasts or immune cells infiltrating into the TME maintain continuous crosstalk with cancer cells and thereby regulate CRC progression. One of the most important molecules involved is the immunoregulatory cytokine transforming growth factor-β (TGFβ). TGFβ is released by various cells in the TME, including macrophages and fibroblasts, and it modulates cancer cell growth, differentiation, and cell death. Mutations in components of the TGF pathway, including TGFβ receptor type 2 or SMAD4, are among the most frequently detected mutations in CRC and have been associated with the clinical course of disease. Within this review, we will discuss our current understanding about the role of TGFβ in the pathogenesis of CRC. This includes novel data on the molecular mechanisms of TGFβ signaling in TME, as well as possible strategies for CRC therapy targeting the TGFβ pathway, including potential combinations with immune checkpoint inhibitors. Full article
(This article belongs to the Special Issue TGF-Beta Signaling in Chronic Inflammation and Cancer: From Immunosuppression to Tissue Remodeling)
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