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Cells
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The TNF Receptor Superfamily in Health and Disease
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The TNF Receptor Superfamily in Health and Disease

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

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 19245

Special Issue Editors

Prof. Dr. Denise Faustman

E-Mail Website
Guest Editor
Massachusetts General Hospital, Boston, USA
Interests: TNF receptor signaling; Type I diabetes; Autoimmunity; Cancer
Dr. Eva S Vanamee

E-Mail Website
Guest Editor
Immunobiology Laboratory, Massachusetts General Hospital, Charlestown, MA 02129, USA
Interests: Structural biology and biophysical methods; TNF superfamily signaling

Special Issue Information

Dear Colleagues,

This Special Issue is meant to collate articles that highlight our current knowledge of the important role that TNF receptor superfamily members play in essential functions such as immune regulation, cell proliferation, cell death, and morphogenesis. Contributions can focus on the signaling mechanism of any TNF receptor superfamily members or downstream signaling partners, their role in health and disease, and therapeutic targeting.

Prof. Dr. Denise Faustman
Guest Editor

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

  • • TNF receptor superfamily • TNF signaling • Apoptosis • Cell proliferation • Cancer • Autoimmunity

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Published Papers (5 papers)

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Research

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11 pages, 1502 KiB  
Communication
LTα, TNF, and ILC3 in Peyer’s Patch Organogenesis
by Violetta S. Gogoleva, Dmitry V. Kuprash, Sergei I. Grivennikov, Alexei V. Tumanov, Andrey A. Kruglov and Sergei A. Nedospasov
Cells 2022, 11(12), 1970; https://doi.org/10.3390/cells11121970 - 19 Jun 2022
Cited by 8 | Viewed by 2821
Abstract
TNF and LTα are structurally related cytokines of the TNF superfamily. Their genes are located in close proximity to each other and to the Ltb gene within the TNF/LT locus inside MHC. Unlike Ltb, transcription of Tnf and of Lta is tightly [...] Read more.
TNF and LTα are structurally related cytokines of the TNF superfamily. Their genes are located in close proximity to each other and to the Ltb gene within the TNF/LT locus inside MHC. Unlike Ltb, transcription of Tnf and of Lta is tightly controlled, with the Tnf gene being an immediate early gene that is rapidly induced in response to various inflammatory stimuli. Genes of the TNF/LT locus play a crucial role in lymphoid tissue organogenesis, although some aspects of their specific contribution remain controversial. Here, we present new findings and discuss the distinct contribution of TNF produced by ILC3 cells to Peyer’s patch organogenesis. Full article
(This article belongs to the Special Issue The TNF Receptor Superfamily in Health and Disease)
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15 pages, 1432 KiB  
Article
Super-Resolution Imaging of Fas/CD95 Reorganization Induced by Membrane-Bound Fas Ligand Reveals Nanoscale Clustering Upstream of FADD Recruitment
by Nicholas Frazzette, Anthony C. Cruz, Xufeng Wu, John A. Hammer, Jennifer Lippincott-Schwartz, Richard M. Siegel and Prabuddha Sengupta
Cells 2022, 11(12), 1908; https://doi.org/10.3390/cells11121908 - 12 Jun 2022
Cited by 5 | Viewed by 3942
Abstract
Signaling through the TNF-family receptor Fas/CD95 can trigger apoptosis or non-apoptotic cellular responses and is essential for protection from autoimmunity. Receptor clustering has been observed following interaction with Fas ligand (FasL), but the stoichiometry of Fas, particularly when triggered by membrane-bound FasL, the [...] Read more.
Signaling through the TNF-family receptor Fas/CD95 can trigger apoptosis or non-apoptotic cellular responses and is essential for protection from autoimmunity. Receptor clustering has been observed following interaction with Fas ligand (FasL), but the stoichiometry of Fas, particularly when triggered by membrane-bound FasL, the only form of FasL competent at inducing programmed cell death, is not known. Here we used super-resolution microscopy to study the behavior of single molecules of Fas/CD95 on the plasma membrane after interaction of Fas with FasL on planar lipid bilayers. We observed rapid formation of Fas protein superclusters containing more than 20 receptors after interactions with membrane-bound FasL. Fluorescence correlation imaging demonstrated recruitment of FADD dependent on an intact Fas death domain, with lipid raft association playing a secondary role. Flow-cytometric FRET analysis confirmed these results, and also showed that some Fas clustering can occur in the absence of FADD and caspase-8. Point mutations in the Fas death domain associated with autoimmune lymphoproliferative syndrome (ALPS) completely disrupted Fas reorganization and FADD recruitment, confirming structure-based predictions of the critical role that these residues play in Fas–Fas and Fas–FADD interactions. Finally, we showed that induction of apoptosis correlated with the ability to form superclusters and recruit FADD. Full article
(This article belongs to the Special Issue The TNF Receptor Superfamily in Health and Disease)
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9 pages, 1442 KiB  
Communication
Signal Amplification in Highly Ordered Networks Is Driven by Geometry
by Éva S. Vanamee, Gábor Lippner and Denise L. Faustman
Cells 2022, 11(2), 272; https://doi.org/10.3390/cells11020272 - 13 Jan 2022
Cited by 4 | Viewed by 2438
Abstract
Here, we hypothesize that, in biological systems such as cell surface receptors that relay external signals, clustering leads to substantial improvements in signaling efficiency. Representing cooperative signaling networks as planar graphs and applying Euler’s polyhedron formula, we can show that clustering may result [...] Read more.
Here, we hypothesize that, in biological systems such as cell surface receptors that relay external signals, clustering leads to substantial improvements in signaling efficiency. Representing cooperative signaling networks as planar graphs and applying Euler’s polyhedron formula, we can show that clustering may result in an up to a 200% boost in signaling amplitude dictated solely by the size and geometry of the network. This is a fundamental relationship that applies to all clustered systems regardless of its components. Nature has figured out a way to maximize the signaling amplitude in receptors that relay weak external signals. In addition, in cell-to-cell interactions, clustering both receptors and ligands may result in maximum efficiency and synchronization. The importance of clustering geometry in signaling efficiency goes beyond biological systems and can inform the design of amplifiers in nonbiological systems. Full article
(This article belongs to the Special Issue The TNF Receptor Superfamily in Health and Disease)
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17 pages, 34727 KiB  
Article
Roles for ADAM17 in TNF-R1 Mediated Cell Death and Survival in Human U937 and Jurkat Cells
by Jürgen Fritsch, Julia Frankenheim, Lothar Marischen, Timea Vadasz, Anja Troeger, Stefan Rose-John, Dirk Schmidt-Arras and Wulf Schneider-Brachert
Cells 2021, 10(11), 3100; https://doi.org/10.3390/cells10113100 - 10 Nov 2021
Cited by 2 | Viewed by 3243
Abstract
Signaling via death receptor family members such as TNF-R1 mediates pleiotropic biological outcomes ranging from inflammation and proliferation to cell death. Pro-survival signaling is mediated via TNF-R1 complex I at the cellular plasma membrane. Cell death induction requires complex IIa/b or necrosome formation, [...] Read more.
Signaling via death receptor family members such as TNF-R1 mediates pleiotropic biological outcomes ranging from inflammation and proliferation to cell death. Pro-survival signaling is mediated via TNF-R1 complex I at the cellular plasma membrane. Cell death induction requires complex IIa/b or necrosome formation, which occurs in the cytoplasm. In many cell types, full apoptotic or necroptotic cell death induction requires the internalization of TNF-R1 and receptosome formation to properly relay the signal inside the cell. We interrogated the role of the enzyme A disintegrin and metalloprotease 17 (ADAM17)/TACE (TNF-α converting enzyme) in death receptor signaling in human hematopoietic cells, using pharmacological inhibition and genetic ablation. We show that in U937 and Jurkat cells the absence of ADAM17 does not abrogate, but rather increases TNF mediated cell death. Likewise, cell death triggered via DR3 is enhanced in U937 cells lacking ADAM17. We identified ADAM17 as the key molecule that fine-tunes death receptor signaling. A better understanding of cell fate decisions made via the receptors of the TNF-R1 superfamily may enable us, in the future, to more efficiently treat infectious and inflammatory diseases or cancer. Full article
(This article belongs to the Special Issue The TNF Receptor Superfamily in Health and Disease)
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Review

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22 pages, 3412 KiB  
Review
The Roles of TNFR2 Signaling in Cancer Cells and the Tumor Microenvironment and the Potency of TNFR2 Targeted Therapy
by Hiroyuki Takahashi, Gumpei Yoshimatsu and Denise Louise Faustman
Cells 2022, 11(12), 1952; https://doi.org/10.3390/cells11121952 - 17 Jun 2022
Cited by 20 | Viewed by 5861
Abstract
The appreciation that cancer growth is promoted by a dynamic tumor microenvironment (TME) has spawned novel approaches to cancer treatment. New therapies include agents that activate quiescent T effector cells and agents that interfere with abnormal neovascularity. Although promising, many experimental therapies targeted [...] Read more.
The appreciation that cancer growth is promoted by a dynamic tumor microenvironment (TME) has spawned novel approaches to cancer treatment. New therapies include agents that activate quiescent T effector cells and agents that interfere with abnormal neovascularity. Although promising, many experimental therapies targeted at the TME have systemic toxicity. Another approach is to target the TME with greater specificity by taking aim at the tumor necrosis factor receptor 2 (TNFR2) signaling pathway. TNFR2 is an attractive molecular target because it is rarely expressed in normal tissues (thus, has low potential for systemic toxicity) and because it is overexpressed on many types of cancer cells as well as on associated TME components, such as T regulatory cells (Tregs), tumor-associated macrophages, and other cells that facilitate tumor progression and spread. Novel therapies that block TNFR2 signaling show promise in cell culture studies, animal models, and human studies. Novel antibodies have been developed that expressly kill only rapidly proliferating cells expressing newly synthesized TNFR2 protein. This review traces the origins of our understanding of TNFR2’s multifaceted roles in the TME and discusses the therapeutic potential of agents designed to block TNFR2 as the cornerstone of a TME-specific strategy. Full article
(This article belongs to the Special Issue The TNF Receptor Superfamily in Health and Disease)
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