TNFR2 expression on non-bone marrow-derived cells is crucial for lipopolysaccharide-induced septic shock and downregulation of soluble TNFR2 level in serum

Liu, Shubai; Rong, Lijie; Deng, Jingjing; Zhao, Xiaopu; Liu, Xiaoman; Xu, Xia; Qin, Zhihai

doi:10.1038/cmi.2010.79

Cited by 5 publications

(2 citation statements)

References 37 publications

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“…It is a pleiotropic cytokine, binds two receptors -TNFR1(receptor type 1: CD120a; p55/60) and TNRFR2 (TNF receptor type 2; CD120b; p75/80)and is produced by many different types of cells (17). Unlike the TNFR2 expression which is limited to immune cells and a few other cell types, TNFR1 expression is present in various cell types (18)(19)(20). TNF-a binds to these receptors resulting in several diverse effects, cell proliferation, survival, and apoptosis (21)(22)(23).…”

Section: Tnf-a Pathway At Glancementioning

confidence: 99%

The Role of Tumor Necrosis Factor in Manipulating the Immunological Response of Tumor Microenvironment

Laha¹,

Grant²,

Mishra³

et al. 2021

Front. Immunol.

107

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The tumor microenvironment (TME) is an intricate system within solid neoplasms. In this review, we aim to provide an updated insight into the TME with a focus on the effects of tumor necrosis factor-α (TNF-α) on its various components and the use of TNF-α to improve the efficiency of drug delivery. The TME comprises the supporting structure of the tumor, such as its extracellular matrix and vasculature. In addition to cancer cells and cancer stem cells, the TME contains various other cell types, including pericytes, tumor-associated fibroblasts, smooth muscle cells, and immune cells. These cells produce signaling molecules such as growth factors, cytokines, hormones, and extracellular matrix proteins. This review summarizes the intricate balance between pro-oncogenic and tumor-suppressive functions that various non-tumor cells within the TME exert. We focused on the interaction between tumor cells and immune cells in the TME that plays an essential role in regulating the immune response, tumorigenesis, invasion, and metastasis. The multifunctional cytokine, TNF-α, plays essential roles in diverse cellular events within the TME. The uses of TNF-α in cancer treatment and to facilitate cancer drug delivery are discussed. The effects of TNF-α on tumor neovasculature and tumor interstitial fluid pressure that improve treatment efficacy are summarized.

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Section: Tnf-a Pathway At Glancementioning

confidence: 99%

The Role of Tumor Necrosis Factor in Manipulating the Immunological Response of Tumor Microenvironment

Laha¹,

Grant²,

Mishra³

et al. 2021

Front. Immunol.

107

View full text Add to dashboard Cite

show abstract

“…TNF receptor 1 (p55 or CD120a) and TNFR2 (p75 or CD120b) are type I transmembrane receptors. TNFR1 shows extensive expression, whereas TNFR2 expression is limited to immune cells and a few other cell types ( 7 , 9 , 10 ). TNFR1 and TNFR2 have similar extracellular TNF-binding structures characterized by four repeated cysteine-rich domains (CRDs) (CRD1 also called pre-ligand binding assembly domain, CRD2, CRD3, and CRD4) but have different intracellular domains ( 11 , 12 ).…”

Section: Tnf Receptor 1 and Tnf Receptormentioning

confidence: 99%

TNF Receptor 2 Makes Tumor Necrosis Factor a Friend of Tumors

Sheng

Qin

2018

Front. Immunol.

Self Cite

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Tumor necrosis factor (TNF) is widely accepted as a tumor-suppressive cytokine via its ubiquitous receptor TNF receptor 1 (TNFR1). The other receptor, TNFR2, is not only expressed on some tumor cells but also on suppressive immune cells, including regulatory T cells and myeloid-derived suppressor cells. In contrast to TNFR1, TNFR2 diverts the tumor-inhibiting TNF into a tumor-advocating factor. TNFR2 directly promotes the proliferation of some kinds of tumor cells. Also activating immunosuppressive cells, it supports immune escape and tumor development. Hence, TNFR2 may represent a potential target of cancer therapy. Here, we focus on expression and role of TNFR2 in the tumor microenvironment. We summarize the recent progress in understanding how TNFR2-dependent mechanisms promote carcinogenesis and tumor growth and discuss the potential value of TNFR2 in cancer treatment.

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IFNγ‐responsiveness of endothelial cells leads to efficient angiostasis in tumours involving down‐regulation of Dll4

Deng

Liu

Rong

et al. 2014

The Journal of Pathology

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Although IFNγ is regarded as a key cytokine in angiostatic response, our poor understanding of its effective cellular target drastically limits its clinical trials against angiogenesis-related disorders. Here, we investigated the effect of IFNγ on endothelial cells (ECs) and possible molecular mechanisms in angiostasis. By employing Tie2(IFNγR) mice, in which IFNγR expression was reconstituted under the control of Tie2 promoter in IFNγR-deficient mice, we found that the response of ECs to IFNγ was highly effective in inhibiting blood supply and retarding tumour growth. Interestingly, the expression of IFNγR on Tie2(-) cells did not inhibit, but promoted tumour growth in control wild-type mice. Mechanism studies showed that IFNγ reacting on ECs down-regulated the delta-like ligand 4 (Dll4)/Notch signalling pathway. Accordingly, overexpression of Dll4 in human ECs diminished the effect of IFNγ on ECs. This study demonstrates that the action of IFNγ on ECs, but not other cells, is highly effective for tumour angiostasis, which involves down-regulating Dll4. It provides insights for EC-targeted angiostatic therapy in treating angiogenesis-associated disorders in the clinic.

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TNFR2 expression on non-bone marrow-derived cells is crucial for lipopolysaccharide-induced septic shock and downregulation of soluble TNFR2 level in serum

Cited by 5 publications

References 37 publications

The Role of Tumor Necrosis Factor in Manipulating the Immunological Response of Tumor Microenvironment

The Role of Tumor Necrosis Factor in Manipulating the Immunological Response of Tumor Microenvironment

TNF Receptor 2 Makes Tumor Necrosis Factor a Friend of Tumors

IFNγ‐responsiveness of endothelial cells leads to efficient angiostasis in tumours involving down‐regulation of Dll4

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