TNF‐mediated inflammatory disease

Bradley, John R.

doi:10.1002/path.2287

Cited by 1,680 publications

(1,376 citation statements)

References 129 publications

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“…TNF-α acts as an endogenous mediator of pro-inflammatory cytokine stimulation and other cellular responses, including lymphocyte activation and migration, and cell proliferation, differentiation and apoptosis [22][23][24].…”

Section: A C C E P T E D Article In Pressmentioning

confidence: 99%

TNF-α inhibitors in asthma and COPD: We must not throw the baby out with the bath water

Matera

Calzetta

Cazzola

2010

Pulmonary Pharmacology & Therapeutics

119

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Tumor necrosis factor (TNF)-α, a pleiotropic cytokine that exerts a variety of effects, such as growth promotion, growth inhibition, angiogenesis, cytotoxicity, inflammation, and immunomodulation, has been implicated in several inflammatory conditions. It plays a significant role in many inflammatory diseases of lung. Given that there is significant literature supporting the pathobiologic role of TNF-α in asthma, mainly in severe refractory asthma, and COPD, TNF-α inhibitors (infliximab, golimumab and etanercept) are now regarded as potential new medications in asthma and COPD management. The studies reported in literature indicate that TNF-α inhibitors are effective in a relatively small subgroup of patients with severe asthma, possibly defined by an increased TNF axis, but they seem to be ineffective in COPD, although an observational study demonstrated that TNF-α inhibitors were associated with a reduction in the rate of COPD hospitalisation among patients with COPD receiving these agents to treat their rheumatoid arthritis. These findings require a smart approach because there is still good reason to target TNF-α, perhaps in a more carefully selected patient group. TNF-α treatment should therefore not be thrown out, or abandoned. Indeed, since severe asthma and COPD are heterogeneous diseases that have characteristics that occur with different phenotypes remained poorly characterized and little known about the underlying pathobiology contributing to them, it is likely that definition of these phenotypes and choice of the right outcome measure will allow us to understand which kind of patients can benefit from TNF-α inhibitors.

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Section: A C C E P T E D Article In Pressmentioning

confidence: 99%

TNF-α inhibitors in asthma and COPD: We must not throw the baby out with the bath water

Matera

Calzetta

Cazzola

2010

Pulmonary Pharmacology & Therapeutics

119

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“…Both TRAIL and TNF‐α have antitumor activity (Aggarwal et al ., 1985; Wiley et al ., 1995) and induce apoptosis (Obeid et al ., 1993; Degli‐Esposti et al ., 1997) albeit by different mechanisms (Jin & El‐Deiry, 2006). Both TRAIL and TNF‐α regulate inflammation (Bradley, 2008), at least partly by regulating a pro‐inflammatory transcription factor NF‐kB (Secchiero et al ., 2003), and both are involved in auto‐immune diseases (Kollias et al ., 1999; Aktas et al ., 2005). Due to these similarities between TRAIL and TNF‐α, the importance of TNF‐α for cochlear pathobiology, and our finding of OPG's importance for survival and function of spiral ganglion neurons (Kao et al ., 2013), we studied the expression and function of TRAIL and DR5 in the inner ear.…”

Section: Introductionmentioning

confidence: 99%

Activation of TRAIL‐DR5 pathway promotes sensorineural degeneration in the inner ear

et al. 2016

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SummaryTumor necrosis factor (TNF) family cytokines are important mediators of inflammation. Elevated levels of serum TNF‐α are associated with human sensorineural hearing loss via poorly understood mechanisms. We demonstrate, for the first time, expression of TNF‐related apoptosis‐inducing ligand (TRAIL) and its signaling death receptor 5 (DR5) in the murine inner ear and show that exogenous TRAIL can trigger hair cell and neuronal degeneration, which can be partly prevented with DR5‐blocking antibodies.

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“…One of the key regulators of inflammation is tumor necrosis factor-α (TNF-α) (Bradley, 2008). Although activated macrophages and T lymphocytes provide the main source of TNF-α in the skin, a wide range of resident skin cells can also produce this cytokine (Metz and Maurer, 2009).…”

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confidence: 99%

“…Although activated macrophages and T lymphocytes provide the main source of TNF-α in the skin, a wide range of resident skin cells can also produce this cytokine (Metz and Maurer, 2009). TNF-α is a modulator of the host response to infection and of programmed cell death, and acts upon the vascular endothelium to increase adhesion and transendothelial migration of leukocytes to sites of inflammation (Bradley, 2008). TNF-α also generates a cytokine cascade that can sensitize cutaneous sensory afferents via at least two pathways.…”

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confidence: 99%

“…Given these properties, it is not surprising that TNF-α plays an important role in various chronic inflammatory diseases, including rheumatoid arthritis, neuropathic pain, inflammatory bowel disease and psoriasis (Bradley, 2008). TNF-α is elevated in the affected tissue of patients with complex regional pain syndrome (CRPS) (Huygen et al, 2002 andBernateck et al, 2010), a chronic pain condition that generally starts after peripheral nerve or tissue injury (Drummond, 2001 andGibbs et al, 2008).…”

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confidence: 99%

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