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Antibodies
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TNF in the Regulation of Immune Cells
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TNF in the Regulation of Immune Cells

A special issue of Antibodies (ISSN 2073-4468).

Deadline for manuscript submissions: closed (31 January 2015) | Viewed by 62225

Special Issue Editor

Dr. Olaf Maier

E-Mail Website
Guest Editor
Institute of Cell Biology and Immunology, Stuttgart University, Allmandring 31, 70569 Stuttgart, Germany
Interests: TNFR2-specific agonists; TNFR2 activation protects neuronal cells against oxidative stress; role of TNF Receptors in neuroinflammation

Special Issue Information

Dear Colleagues,

The cytokine tumor necrosis factor (TNF) is a master regulator of the immune system and its role in the regulation of the innate, as well as the adaptive, immune system; mainly the regulation of T cell activity, has been firmly established. As such, TNF plays an important role in the immune response against a variety of pathogens. Due to its potency, TNF must be tightly regulated and deregulation of TNF signaling can lead to chronic inflammation, and has been implicated in various diseases ranging from autoimmune diseases to neurodegenerative diseases and cancer. Importantly, anti-TNF treatment has been successful in various autoimmune diseases verifying the concept that sustained TNF activation is an important mediator of chronic inflammation and autoimmune disease. However, it has become evident that, depending on the context, TNF signaling can be highly diverse, ranging from pro- to anti-inflammatory and is regenerative. Here, the different forms of TNF, i.e., membrane-bound versus soluble, as well as the distinct signaling of the two TNF receptors, TNFR1 and TNFR2, are of major relevance. TNF availability is further modulated by the shedding of TNF receptor ectodomains, which may act as antagonists or as TNF storage pools. Studies with dominant-negative TNF have shown that it is predominantly the soluble form of TNF that is pro-inflammatory. Moreover, since soluble TNF acts primarily via TNFR1, this receptor is implicated in the pro-inflammatory signaling of TNF. In contrast, TNFR2 has been associated with tissue regeneration and immune modulation. Here, the recent observation that TNFR2 can promote the activity of regulatory T cells is of major importance for our understanding of the role of TNF in immune cell regulation.

This Special Issue will focus on the role of TNF in the regulation of immune cells. Welcome are contributions that address and review the role of TNF and its receptors in the regulation of the innate and/or adaptive immune system, as well as the role of deregulation of TNF signaling in disease.

Dr. Olaf Maier
Guest Editor

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 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 regulation of the innate immune system
  • TNF regulation of the adaptive immune system
  • TNF signaling pathways in the regulation of immune cells
  • regulation of TNF expression
  • soluble and membrane-bound TNF
  • soluble TNF receptor ectodomains
  • TNFR2 and regulatory T cells
  • TNF in autoimmune diseases
  • TNF in neurodegenerative diseases
  • TNF signaling and cancer
  • TNF antagonists as therapeutics
  • TNF receptor specific (ant)agonists as therapeutics

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Published Papers (4 papers)

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Research

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1262 KiB  
Article
Reverse Signaling Contributes to Control of Chronic Inflammation by Anti-TNF Therapeutics
by Orsolya Sipos, Annamária Török, Tanja Kalic, Ernő Duda and Kata Filkor
Antibodies 2015, 4(2), 123-140; https://doi.org/10.3390/antib4020123 - 9 Jun 2015
Cited by 5 | Viewed by 7983
Abstract
Anti-tumor necrosis factor (TNF) monoclonal antibodies and TNF receptor ectodomain fusion protein are in clinical use to neutralize circulating TNF and ameliorate symptoms of many autoimmune diseases and pathological conditions with chronic inflammation. In this paper we present data to prove that reverse [...] Read more.
Anti-tumor necrosis factor (TNF) monoclonal antibodies and TNF receptor ectodomain fusion protein are in clinical use to neutralize circulating TNF and ameliorate symptoms of many autoimmune diseases and pathological conditions with chronic inflammation. In this paper we present data to prove that reverse signaling, elicited by agonist molecules interacting with the membrane-bound TNF of myeloid cells, significantly contributes to the therapeutic effect of these anti-TNF medicines. Interaction of agonist monoclonals with cell surface TNF significantly attenuates the expression of pro-inflammatory cytokines and induces changes in the production of extracellular and intracellular signaling molecules. This phenomenon is not dependent on the Fc portion of antibodies as Fab constructs are as efficient as full antibody molecules. Full article
(This article belongs to the Special Issue TNF in the Regulation of Immune Cells)
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988 KiB  
Article
TNFR1 and TNFR2 Expression and Induction on Human Treg Cells from Type 1 Diabetic Subjects
by Melanie Heinrich, Douglas Burger, Limei Wang, Georges Tahhan, Peter Reinhold III, Menghan Zhao, Elise Hsu, Sarah Warden, Danielle Baum and Denise L Faustman
Antibodies 2015, 4(1), 34-47; https://doi.org/10.3390/antib4010034 - 3 Mar 2015
Cited by 5 | Viewed by 8944
Abstract
Several autoimmune diseases are marked by a deficiency of soluble tumor necrosis factor (TNF). The TNF deficiency is caused in at least one autoimmune disease, multiple sclerosis, by an overabundance of TNF receptor 1 (TNFR1). Excess TNFR1 binds and inactivates TNF and this [...] Read more.
Several autoimmune diseases are marked by a deficiency of soluble tumor necrosis factor (TNF). The TNF deficiency is caused in at least one autoimmune disease, multiple sclerosis, by an overabundance of TNF receptor 1 (TNFR1). Excess TNFR1 binds and inactivates TNF and this leaves less TNF bioavailable. This study sought to determine if expression of fresh or IL2-stimulated TNF receptors on Tregs cells, an important immunoregulatory cell involved in autoimmunity, is altered in type I diabetes. Standard fluorescence analysis was used to examine the levels of TNFR1 and TNFR2 on human Tregs in patients with type I diabetes (T1D) or controls. Fresh Tregs from T1D compared to control Tregs had identical levels of TNFR1. In marked contrast, Type 1 diabetic patients Treg cells had statistically elevated levels of TNFR2 compared to controls. Tregs stimulated with IL2 from both T1D and controls showed marked increase of TNFR2 expression in a dose-response manner, but the dose response increase in TNFR2 was significantly higher for T1D Treg cells. No IL2 dose-response was present for TNFR1 on either T1D or control Tregs exposed to IL2. A large study of serum for secreted levels of TNFR2 also revealed elevated circulating levels consistent with the elevated surface expression on Tregs. These findings suggest that abnormal regulation of TNFR2 expression with elevated cellular and secreted levels of TNFR2 is a characteristic of Type 1 diabetes. It is possible that the relative deficiency of TNF in type I diabetes, in contrast to multiple sclerosis, is caused by excess expression of TNFR such as TNFR2, a binding structure for inactivating TNF. Full article
(This article belongs to the Special Issue TNF in the Regulation of Immune Cells)
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Review

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1569 KiB  
Review
Targeting of Tumor Necrosis Factor Alpha Receptors as a Therapeutic Strategy for Neurodegenerative Disorders
by Yun Dong, Doortje W. Dekens, Peter Paul De Deyn, Petrus J. W. Naudé and Ulrich L. M. Eisel
Antibodies 2015, 4(4), 369-408; https://doi.org/10.3390/antib4040369 - 19 Nov 2015
Cited by 35 | Viewed by 22842
Abstract
Numerous studies have revealed the pleiotropic functions of tumor necrosis factor alpha (TNF-α), and have linked it with several neurodegenerative disorders. This review describes the signaling pathways induced by TNF-α via its two receptors (TNFR1 and TNFR2), and their functions in neurodegenerative processes [...] Read more.
Numerous studies have revealed the pleiotropic functions of tumor necrosis factor alpha (TNF-α), and have linked it with several neurodegenerative disorders. This review describes the signaling pathways induced by TNF-α via its two receptors (TNFR1 and TNFR2), and their functions in neurodegenerative processes as in Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis (MS), and ischemic stroke. It has become clear that TNF-α may exert divergent actions in neurodegenerative disorders, including neurodegenerative and neuroprotective effects, which appear to depend on its signaling via either TNFR1 or TNFR2. Specific targeting of these receptors is a promising therapeutic strategy for many disorders. Full article
(This article belongs to the Special Issue TNF in the Regulation of Immune Cells)
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775 KiB  
Review
Targeting sTNF/TNFR1 Signaling as a New Therapeutic Strategy
by Roman Fischer, Roland E. Kontermann and Olaf Maier
Antibodies 2015, 4(1), 48-70; https://doi.org/10.3390/antib4010048 - 6 Mar 2015
Cited by 70 | Viewed by 21652
Abstract
Deregulation of the tumor necrosis factor (TNF) plays an important role in the initiation and perpetuation of chronic inflammation and has been implicated in the development of various autoimmune diseases. Accordingly, TNF-inhibitors are successfully used for the treatment of several diseases, such as [...] Read more.
Deregulation of the tumor necrosis factor (TNF) plays an important role in the initiation and perpetuation of chronic inflammation and has been implicated in the development of various autoimmune diseases. Accordingly, TNF-inhibitors are successfully used for the treatment of several diseases, such as rheumatoid arthritis, inflammatory bowel disease, and psoriasis. However, total inhibition of TNF can cause severe side effects such as an increased risk of inflammation and reactivation of tuberculosis. This is likely due to the different actions of the two TNF receptors. Whereas TNFR1 predominantly promotes inflammatory signaling pathways, TNFR2 mediates immune modulatory functions and promotes tissue homeostasis and regeneration. Therefore, the specific blockage of TNFR1 signaling, either by direct inhibition with TNFR1-selective antagonists or by targeting soluble TNF, which predominantly activates TNFR1, may prevent the detrimental effects associated with total TNF-inhibitors and constitute a next-generation approach to interfere with TNF. Full article
(This article belongs to the Special Issue TNF in the Regulation of Immune Cells)
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