Soluble tumor necrosis factor receptors as predictors of 1-year mortality and renal dysfunction after liver transplantation

Morais, Bruno; Teixeira, Antônio Lúcio; Maciel, Jader F.; Lima, Alessandro Rodrigues; Barbosa, Izabela Guimarães; Sanches, Marcelo Dias

doi:10.1016/j.trim.2016.01.006

Cited by 6 publications

(4 citation statements)

References 28 publications

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“…Elevated sTNFR1 (but not sTNFR2) was associated with worse outcomes when presenting to an emergency room with shortness of breath, but also lost statistical significance when adjusting for CRP ( 125 ). Associations unique to sTNFR1 were also seen with treatment-responsive lupus ( 122 ), sleep disruption in depression ( 119 ), worse outcomes in GVHD after ablative-conditioned BMT ( 129 ), and mortality and dialysis needs for post-liver transplant patients ( 120 ). Two studies have assessed the expression of TNFR1 versus TNFR2 on immune cells ( 121 , 123 ), compared to healthy controls: patients with atopic dermatitis have increased expression of TFNR1 on their T-cells ( 121 ); patients with hypersensitivity pneumonitis have elevated TNFR1 expression on alveolar macrophages but elevated TNFR2 on peripheral lymphocytes ( 123 ).…”

Section: Differential Soluble and Tissue Tnfr Associations In Diseasementioning

confidence: 99%

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

2020

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Since its discovery in 1975, TNFα has been a subject of intense study as it plays significant roles in both immunity and cancer. Such attention is well deserved as TNFα is unique in its engagement of pleiotropic signaling via its two receptors: TNFR1 and TNFR2. Extensive research has yielded mechanistic insights into how a single cytokine can provoke a disparate range of cellular responses, from proliferation and survival to apoptosis and necrosis. Understanding the intracellular signaling pathways induced by this single cytokine via its two receptors is key to further revelation of its exact functions in the many disease states and immune responses in which it plays a role. In this review, we describe the signaling complexes formed by TNFR1 and TNFR2 that lead to each potential cellular response, namely, canonical and non-canonical NF-κB activation, apoptosis and necrosis. This is followed by a discussion of data from in vivo mouse and human studies to examine the differential impacts of TNFR1 versus TNFR2 signaling.

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Section: Differential Soluble and Tissue Tnfr Associations In Diseasementioning

confidence: 99%

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

2020

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“…As a result of cellular activation by TNFα, alternative splicing of mRNA occurs resulting in the production of soluble TNFR which is detectable in the blood (110). Serum TNFR-1 and -2 levels have been shown to be independent predictors of AKI, severe AKI, need for kidney replacement therapy, and mortality and elevated TNFR-1 has been shown to be a marker of slower kidney recovery (109,(111)(112)(113)(114)(115). In a study of patients with COVID-19, patients were found to have increasing levels of TNFR-1 and TNFR-2 with increasing stage of AKI (114).…”

Section: Tnfr-1 and Tnfr-2mentioning

confidence: 99%

Update on prognosis driven classification of pediatric AKI

Patel

Gbadegesin²

2022

Front. Pediatr.

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Acute kidney injury (AKI) affects a large proportion of hospitalized children and increases morbidity and mortality in this population. Initially thought to be a self-limiting condition with uniformly good prognosis, we now know that AKI can persist and progress to acute kidney disease (AKD) and chronic kidney disease (CKD). AKI is presently categorized by stage of injury defined by increase in creatinine, decrease in eGFR, or decrease in urine output. These commonly used biomarkers of acute kidney injury do not change until the injury is well established and are unable to detect early stage of the disease when intervention is likely to reverse injury. The kidneys have the ability to compensate and return serum creatinine to a normal or baseline level despite nephron loss in the setting of AKI possibly masking persistent dysfunction. Though these definitions are important, classifying children by their propensity for progression to AKD and CKD and defining these risk strata by other factors besides creatinine may allow for better prognosis driven discussion, expectation setting, and care for our patients. In order to develop a classification strategy, we must first be able to recognize children who are at risk for AKD and CKD based on modifiable and non-modifiable factors as well as early biomarkers that identify their risk of persistent injury. Prevention of initial injury, prompt evaluation and treatment if injury occurs, and mitigating further injury during the recovery period may be important factors in decreasing risk of AKD and CKD after AKI. This review will cover presently used definitions of AKI, AKD, and CKD, recent findings in epidemiology and risk factors for AKI to AKD to CKD progression, novel biomarkers for early identification of AKI and AKI that may progress to CKD and future directions for improving outcome in children with AKI.

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“…Signaling mediated via mTNF is further bifunctional, for example, promoting increased TNF production and, at the same time, a negative regulatory response via secretion of TGF-ß, which promoted resistance to LPS-induced inflammation in macrophages [21][22][23][24][25]. Albeit the function of TNFR2 was extensively studied on DCs, monocytes, and T cells [22,[26][27][28][29], and there is evidence that soluble TNFR2 could be used as a biomarker in a variety of inflammatory disease states [30][31][32], the role of this receptor on human B cells remains to be investigated. As demonstrated earlier by our group, TNFR2 expression is inducible on a variety of peripheral B-cell subpopulations and its presence coincides with TLR9-triggered formation of IL-10 and antibody-secreting B cells [33].…”

Section: Introductionmentioning

confidence: 99%

TNFR2 expression is a hallmark of human memory B cells with suppressive function

et al. 2021

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Tumor Necrosis Factor Receptor 2 (TNFR2) expression is increasingly being linked to tolerogenic immune reactions and cells with suppressor function including a subset of T-regulatory cells. B-regulatory cells play an important role in control of T-cell responsesand inflammation. Recently, we described TNFR2 as a marker for IL-10-producing B cells, a hallmark of this cell subset. Here, we demonstrate that proliferation of T cells is reduced in the presence of TNFR2 positive human memory B cells generated with TLR9 ligand, while TNFR2-and TNFR2+CD27-B cells display costimulatory activity. Our data further reveal that IL-10 secretion is characteristic of IgM+ naïve and memory B cells but suppressive activity is not restricted to IL-10: (i) the inhibitory effect of TNFR2+ switched memory B cells was comparable to that exerted by TNFR2+ IgM+ memory B cells although IL-10 secretion levels in the cocultures were lower; (ii) supernatants from TNFR2+ memory B cells failed to suppress T-cell proliferation. Based on our findings, we propose that formation of Breg is a specific characteristic of human memory B cells undergoing terminal differentiation. Our data further corroborate that TNFR2 represents a viable marker for identification of memory B cells with regulatory function.

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Soluble tumor necrosis factor receptors as predictors of 1-year mortality and renal dysfunction after liver transplantation

Cited by 6 publications

References 28 publications

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

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

Update on prognosis driven classification of pediatric AKI

TNFR2 expression is a hallmark of human memory B cells with suppressive function

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