Tumor Necrosis Factor Receptors: Pleiotropic Signaling Complexes and Their Differential Effects

Gough, Portia; Myles, Ian A.

doi:10.3389/fimmu.2020.585880

Cited by 153 publications

(146 citation statements)

References 166 publications

(177 reference statements)

Supporting

Mentioning

127

Contrasting

Unclassified

Order By: Relevance

“…However, TNFα has a dual role in cell survival/cell death via different signalling pathways depending on its receptors, TNFR1 and TNFR2 [59]. Whereas TNFR1 is mainly involved in inflammation and neurodegenerative processes, TNFR2 contributes to cell regeneration and neuroprotection [17,20,59]. Since in the duodenum of diabetic rats the total number of myenteric neurons remained unchanged [6], we presumed that an increased duodenal TNFα expression may have participated in neuroprotection here.…”

Section: Discussionmentioning

confidence: 84%

See 1 more Smart Citation

Intestinal Region-Specific and Layer-Dependent Induction of TNFα in Rats with Streptozotocin-Induced Diabetes and after Insulin Replacement

Bódi

Chandrakumar

Doghmi

et al. 2021

Cells

View full text Add to dashboard Cite

Tumour necrosis factor alpha (TNFα) is essential in neuroinflammatory modulation. Therefore, the goal of this study is to reveal the effects of chronic hyperglycaemia and insulin treatment on TNFα expression in different gut segments and intestinal wall layers. TNFα expression was mapped by fluorescent immunohistochemistry and quantitative immunogold electron microscopy in myenteric ganglia of duodenum, ileum and colon. Tissue TNFα levels were measured by enzyme-linked immunosorbent assays in muscle/myenteric plexus-containing (MUSCLE-MP) and mucosa/submucosa/submucous plexus-containing (MUC-SUBMUC-SP) homogenates. Increasing density of TNFα-labelling gold particles is observed in myenteric ganglia from proximal to distal segments and TNFα tissue levels are much more elevated in MUSCLE-MP homogenates than in MUC-SUBMUC-SP samples in healthy controls. In the diabetics, the number of TNFα gold labels is significantly increased in the duodenum, decreased in the colon and remained unchanged in the ileal ganglia, while insulin does not prevent these diabetes-related TNFα changes. TNFα tissue concentration is also increased in MUSCLE-MP homogenates of diabetic duodenum, while decreased in MUC-SUBMUC-SP samples of diabetic ileum and colon. These findings support that type 1 diabetes has region-specific and intestinal layer-dependent effects on TNFα expression, contributing to the regional damage of myenteric neurons and their intestinal milieu.

show abstract

Section: Discussionmentioning

confidence: 84%

Section: Discussionmentioning

confidence: 99%

Intestinal Region-Specific and Layer-Dependent Induction of TNFα in Rats with Streptozotocin-Induced Diabetes and after Insulin Replacement

Bódi

Chandrakumar

Doghmi

et al. 2021

Cells

View full text Add to dashboard Cite

show abstract

“…TNFR1 is widely expressed on most cells and is both proinflammatory and apoptotic. TNRF2 expression is limited mainly to endothelial cells and certain immunocytes and participates in anti-inflammatory processes and cell proliferation (99,100). Proteolytic cleavage produces soluble forms of TNFR (sTNFR).…”

Section: Tnfr2mentioning

confidence: 99%

Alternative Splicing: A New Cause and Potential Therapeutic Target in Autoimmune Disease

Ren

Cai

et al. 2021

Front. Immunol.

View full text Add to dashboard Cite

Alternative splicing (AS) is a complex coordinated transcriptional regulatory mechanism. It affects nearly 95% of all protein-coding genes and occurs in nearly all human organs. Aberrant alternative splicing can lead to various neurological diseases and cancers and is responsible for aging, infection, inflammation, immune and metabolic disorders, and so on. Though aberrant alternative splicing events and their regulatory mechanisms are widely recognized, the association between autoimmune disease and alternative splicing has not been extensively examined. Autoimmune diseases are characterized by the loss of tolerance of the immune system towards self-antigens and organ-specific or systemic inflammation and subsequent tissue damage. In the present review, we summarized the most recent reports on splicing events that occur in the immunopathogenesis of systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) and attempted to clarify the role that splicing events play in regulating autoimmune disease progression. We also identified the changes that occur in splicing factor expression. The foregoing information might improve our understanding of autoimmune diseases and help develop new diagnostic and therapeutic tools for them.

show abstract

“…IFN-α significantly inhibits hormone secretion and intracellular hormone concentration in human GH secreting PAs, prolactin, and NFPAs or gonadotropin adenoma [ 63 ]. TNF can trigger a variety of potential outcomes through TNFR1 and TNFR2 activation signals, including cell proliferation, gene activation, or cell death [ 64 ]. In invasive PAs, TNF-α promotes pathological osteoclast formation by directly inducing osteoclast differentiation, leading to inflammatory bone destruction [ 65 ].…”

Section: Inflammatory Factors Associated With Pasmentioning

confidence: 99%

Research advances on the immune research and prospect of immunotherapy in pituitary adenomas

Nie

Fang

et al. 2021

World J Surg Onc

View full text Add to dashboard Cite

Background Pituitary adenomas are one type of intracranial tumor, which can be divided into microadenoma (≤ 1 cm), macroadenoma (> 1 cm), and giant adenoma (≥ 4 cm) according to their diametral sizes. They are benign, typically slow-progressing, whereas the biological behavior of some of them is invasive, which presents a major clinical challenge. Treatment of some pituitary adenomas is still difficult due to drug resistance or multiple relapses, usually after surgery, medication, and radiation. At present, no clear prediction and treatment biomarkers have been found in pituitary adenomas and some of them do not cause clinical symptoms, so patients are often found to be ill through physical examination, and some are even found through autopsy. With the development of research on pituitary adenomas, the immune response has become a hot spot and may serve as a novel disease marker and therapeutic target. The distribution and function of immune cells and their secreted molecules in pituitary adenomas are extremely complex. Researchers found that infiltration of immune cells may have a positive effect on the treatment and prognosis of pituitary adenomas. In this review, we summarized the advance of tumor immunity in pituitary adenomas, revealing the immunity molecules as potential biomarkers as well as therapeutic agents for pituitary adenomas. Conclusion The immune studies related to pituitary adenomas may help us find relevant immune markers. At the same time, the exploration of immunotherapy also provides new options for the treatment of pituitary adenomas.

show abstract

Tumor Necrosis Factor Receptors: Pleiotropic Signaling Complexes and Their Differential Effects

Cited by 153 publications

References 166 publications

Intestinal Region-Specific and Layer-Dependent Induction of TNFα in Rats with Streptozotocin-Induced Diabetes and after Insulin Replacement

Intestinal Region-Specific and Layer-Dependent Induction of TNFα in Rats with Streptozotocin-Induced Diabetes and after Insulin Replacement

Alternative Splicing: A New Cause and Potential Therapeutic Target in Autoimmune Disease

Research advances on the immune research and prospect of immunotherapy in pituitary adenomas

Contact Info

Product

Resources

About