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Cells
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Demystifying the Role of the Immune System in Modulating Pathogenic...
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Demystifying the Role of the Immune System in Modulating Pathogenic Fibrosis

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

Deadline for manuscript submissions: 31 January 2025 | Viewed by 2218

Special Issue Editors

Dr. Gerlinde Wernig

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Guest Editor
Department of Pathology, School of Medicine, Stanford University, Stanford, CA, USA
Interests: innate immunity; fibrosis; genetic reprogramming of fibrotic niches
Special Issues, Collections and Topics in MDPI journals
Dr. Cristabelle De Souza

E-Mail Website
Guest Editor
Department of Stem Cell Research and Regenerative Medicine, Department of Pathology, School of Medicine, Stanford University, Stanford, CA 94305, USA
Interests: cancer immunology; molecular therapeutics; translational medicine; functional genomics and small molecule inhibitors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Fibrotic diseases are not well understood. Severe end-stage fibrosis is characterized by the development of organ fibrosis without known etiologies, with devastating disease outcomes like idiopathic pulmonary fibrosis, scleroderma, liver cirrhosis, NASH, and diabetic nephropathy among others. These diseases have a poor prognosis comparable with end-stage cancer and are uncurable. Given the phenotypic differences, different fibrotic diseases also have different pathomechanisms. However, the role of the immune system in modulating this pathogenesis is still unknown.  In this issue, we would like to focus on understanding different end stage fibrotic diseases—including IPF, scleroderma, myelofibrosis, kidney, pancreas, and heart fibrosis, and nonalcoholic steatohepatitis—to discover specific mechanisms and pathways that can be targeted for therapeutic intervention.
This Special Issue is focused on the immune regulatory molecules that drive pathogenic fibrosis and the mechanisms that drive the progression of fibrosis to cancer. We welcome original research and review articles pertaining to the following areas:

  • Novel genetic markers that can regulate immune molecules in fibrotic diseases;
  • Studies identifying novel immune markers and mechanisms driving the fibrotic phenotype in multiple organ types;
  • Studies that have identified novel immune biomarkers that can predict disease severity;
  • Studies that are focused on drug discovery, development, and target validation in the realm of fibrotic diseases.

We look forward to receiving your contributions.

Dr. Gerlinde Wernig
Dr. Cristabelle De Souza
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • unifying fibrotic mechanisms
  • genetic markers of disease
  • innate immunity
  • drug discovery

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Published Papers (1 paper)

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Research

17 pages, 19526 KiB  
Article
Novel Vitamin D3 Hydroxymetabolites Require Involvement of the Vitamin D Receptor or Retinoic Acid-Related Orphan Receptors for Their Antifibrogenic Activities in Human Fibroblasts
by Zorica Janjetovic, Shariq Qayyum, Sivani B. Reddy, Ewa Podgorska, S. Gates Scott, Justyna Szpotan, Alisa A. Mobley, Wei Li, Vijay K. Boda, Senthilkumar Ravichandran, Robert C. Tuckey, Anton M. Jetten and Andrzej T. Slominski
Cells 2024, 13(3), 239; https://doi.org/10.3390/cells13030239 - 26 Jan 2024
Cited by 5 | Viewed by 1787
Abstract
We investigated multiple signaling pathways activated by CYP11A1-derived vitamin D3 hydroxymetabolites in human skin fibroblasts by assessing the actions of these molecules on their cognate receptors and by investigating the role of CYP27B1 in their biological activities. The actions of 20(OH)D3, 20,23(OH)2 [...] Read more.
We investigated multiple signaling pathways activated by CYP11A1-derived vitamin D3 hydroxymetabolites in human skin fibroblasts by assessing the actions of these molecules on their cognate receptors and by investigating the role of CYP27B1 in their biological activities. The actions of 20(OH)D3, 20,23(OH)2D3, 1,20(OH)2D3 and 1,20,23(OH)3D3 were compared to those of classical 1,25(OH)2D3. This was undertaken using wild type (WT) fibroblasts, as well as cells with VDR, RORs, or CYP27B1 genes knocked down with siRNA. Vitamin D3 hydroxymetabolites had an inhibitory effect on the proliferation of WT cells, but this effect was abrogated in cells with silenced VDR or RORs. The collagen expression by WT cells was reduced upon secosteroid treatment. This effect was reversed in cells where VDR or RORs were knocked down where the inhibition of collagen production and the expression of anti-fibrotic genes in response to the hydroxymetabolites was abrogated, along with ablation of their anti-inflammatory action. The knockdown of CYP27B1 did not change the effect of either 20(OH)D3 or 20,23(OH)2D3, indicating that their actions are independent of 1α-hydroxylation. In conclusion, the expression of the VDR and/or RORα/γ receptors in fibroblasts is necessary for the inhibition of both the proliferation and fibrogenic activity of hydroxymetabolites of vitamin D3, while CYP27B1 is not required. Full article
(This article belongs to the Special Issue Demystifying the Role of the Immune System in Modulating Pathogenic Fibrosis)
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