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https://www.readbyqxmd.com/read/29109283/sirp%C3%AE-dendritic-cells-regulate-homeostasis-of-fibroblastic-reticular-cells-via-tnf-receptor-ligands-in-the-adult-spleen
#1
Yasuyuki Saito, Datu Respatika, Satomi Komori, Ken Washio, Taichi Nishimura, Takenori Kotani, Yoji Murata, Hideki Okazawa, Hiroshi Ohnishi, Yoriaki Kaneko, Katsuyuki Yui, Koji Yasutomo, Chikako Nishigori, Yoshihisa Nojima, Takashi Matozaki
In secondary lymphoid organs, development and homeostasis of stromal cells such as podoplanin (Pdpn)-positive fibroblastic reticular cells (FRCs) are regulated by hematopoietic cells, but the cellular and molecular mechanisms of such regulation have remained unclear. Here we show that ablation of either signal regulatory protein α (SIRPα), an Ig superfamily protein, or its ligand CD47 in conventional dendritic cells (cDCs) markedly reduced the number of CD4(+) cDCs as well as that of Pdpn(+) FRCs and T cells in the adult mouse spleen...
November 6, 2017: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29109120/cd27-mediated-regulatory-t-cell-depletion-and-effector-t-cell-costimulation-both-contribute-to-antitumor-efficacy
#2
Anna Wasiuk, James Testa, Jeff Weidlick, Crystal Sisson, Laura Vitale, Jenifer Widger, Andrea Crocker, Lawrence J Thomas, Joel Goldstein, Henry C Marsh, Tibor Keler, Li-Zhen He
CD27, a member of the TNFR superfamily, is constitutively expressed in most T cells and plays crucial roles in T cell effector functions. The costimulation and antitumor activity of CD27 agonistic Abs have been well documented in mouse models. Clinical testing of a human IgG1 anti-CD27 Ab, varlilumab (clone 1F5), is ongoing in cancer patients. In this study, we set out to further understand CD27 as an immunomodulatory target and to address the mechanism of antitumor efficacy using different IgG isotypes of 1F5 in human CD27-transgenic mice...
November 6, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29108854/socs-1-ameliorates-smoke-inhalation-induced-acute-lung-injury-through-inhibition-of-ask-1-activity-and-disc-formation
#3
Leifang Zhang, Kairei Zhu, Yating Ma, Chenming Xu, Qiwen Shi, Xiaoming Chen, Weike Su, Hang Zhao
Smoke inhalation leads to acute lung injury (ALI), a devastating clinical problem associated with high mortality. Suppressor of cytokine signaling-1 (SOCS-1) is a negative regulator of apoptosis and pro-inflammatory cytokine signaling, two major contributors to the pathogenesis of ALI. We have found that SOCS-1 protects lung epithelial cells from smoke-induced apoptosis through two mechanisms. One is that SOCS-1 enhances degradation of ASK-1 and diminishes cleavage of pro-caspase-3 to repress smoke-triggered apoptosis in lung epithelial cells...
November 3, 2017: Clinical Immunology: the Official Journal of the Clinical Immunology Society
https://www.readbyqxmd.com/read/29066276/signaling-by-cell-surface-death-receptors-alterations-in-head-and-neck-cancer
#4
REVIEW
Brandon C Leonard, Daniel E Johnson
Cell surface death receptors are members of the tumor necrosis factor receptor (TNFR) superfamily and mediate signals leading to the induction of apoptosis or necroptosis, as well as NF-κB-mediated cell survival. These biochemical processes play key roles in cell growth, development, tissue homeostasis, and immune responses. The downstream signaling complexes activated by different death receptors can differ significantly and are subject to multiple, distinct regulatory mechanisms. Dysregulation of signaling by the TNFR superfamily contributes to a variety of pathologic conditions, including defective immune responses and cancer...
October 18, 2017: Advances in Biological Regulation
https://www.readbyqxmd.com/read/29062811/activation-of-nf-kb-mediated-tnf-induced-antimicrobial-immunity-is-required-for-the-efficient-brucella-abortus-clearance-in-raw-264-7-cells
#5
Huynh T Hop, Alisha W B Reyes, Tran X N Huy, Lauren T Arayan, WonGi Min, Hu J Lee, Man H Rhee, Hong H Chang, Suk Kim
In this study, we explore the regulatory roles of pro-inflammatory cytokine tumor necrosis factor alpha (TNF) in the innate immunity of macrophages against B. abortus infection. We show that infection of macrophage with B. abortus induces marked expression and secretion of TNF which subsequently binds to TNF receptor 1 (TNFR-1) and activates a downstream signaling cascade of the innate immunity. Blocking of TNF signaling resulted in a notable increase of B. abortus survival which was associated with an increase of anti-inflammatory cytokine interleukin 10 (IL-10), a beneficial effector of Brucella survival, as well as remarkable decrease of reactive oxygen species (ROS) and nitric oxide (NO), antibrucella molecules...
2017: Frontiers in Cellular and Infection Microbiology
https://www.readbyqxmd.com/read/29052145/cell-death-pathways-a-novel-therapeutic-approach-for-neuroscientists
#6
REVIEW
G Morris, A J Walker, M Berk, M Maes, B K Puri
In the first part, the following mechanisms involved in different forms of cell death are considered, with a view to identifying potential therapeutic targets: tumour necrosis factor receptors (TNFRs) and their engagement by tumour necrosis factor-alpha (TNF-α); poly [ADP-ribose] polymerase (PARP)-1 cleavage; the apoptosis signalling kinase (ASK)-c-Jun N-terminal kinase (JNK) axis; lysosomal permeability; activation of programmed necrotic cell death; oxidative stress, caspase-3 inhibition and parthanatos; activation of inflammasomes by reactive oxygen species and the development of pyroptosis; oxidative stress, calcium dyshomeostasis and iron in the development of lysosomal-mediated necrosis and lysosomal membrane permeability; and oxidative stress, lipid peroxidation, iron dyshomeostasis and ferroptosis...
October 19, 2017: Molecular Neurobiology
https://www.readbyqxmd.com/read/29038485/a-versatile-pretargeting-approach-for-tumour-selective-delivery-and-activation-of-tnf-superfamily-members
#7
Yuan He, Peter E van Bommel, Douwe F Samplonius, Edwin Bremer, Wijnand Helfrich
TNFR superfamily (TNFRSF) members have important immunoregulatory functions and are of clear interest for cancer immunotherapy. Various TNFRSF agonists have been clinically evaluated, but have met with limited efficacy and/or toxicity. Recent insights indicate that 'first-generation' TNFRSF agonists lack efficacy as they do not effectively cross-link their corresponding receptor. Reversely, ubiquitous TNFRSF receptor(s) cross-linking by CD40 and Fas agonistic antibodies resulted in dose-limiting liver toxicity...
October 16, 2017: Scientific Reports
https://www.readbyqxmd.com/read/29038250/inhibition-of-irak1-ubiquitination-determines-glucocorticoid-sensitivity-for-tlr9-induced-inflammation-in-macrophages
#8
Fansheng Kong, Zhiwei Liu, Viral G Jain, Kenjiro Shima, Takuji Suzuki, Louis J Muglia, Daniel T Starczynowski, Chandrashekhar Pasare, Sandip Bhattacharyya
Inflammatory responses are controlled by signaling mediators that are regulated by various posttranslational modifications. Recently, transcription-independent functions for glucocorticoids (GC) in restraining inflammation have emerged, but the underlying mechanisms are unknown. In this study, we report that GC receptor (GR)-mediated actions of GC acutely suppress TLR9-induced inflammation via inhibition of IL-1R-associated kinase 1 (IRAK1) ubiquitination. β-TrCP-IRAK1 interaction is required for K48-linked ubiquitination of IRAK1 at Lys(134) and subsequent membrane-to-cytoplasm trafficking of IRAK1 interacting partners TNFR-associated factor 6 and TAK1 that facilitates NF-κB and MAPK activation...
November 15, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29037450/tissue-expression-of-tubular-injury-markers-is-associated-with-renal-function-decline-in-diabetic-nephropathy
#9
Subin Hwang, Jeeeun Park, Jinhae Kim, Hye Ryoun Jang, Ghee Young Kwon, Wooseong Huh, Yoon-Goo Kim, Dae Joong Kim, Ha Young Oh, Jung Eun Lee
AIMS: The pathogenesis of diabetic kidney disease (DKD) is complex and multifactorial; increasing evidence suggests that tubular injury and inflammatory process are involved in disease progression. We investigated the potential association of renal expression of tubular injury markers, neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and inflammatory markers, tumor necrosis factor receptor (TNFR) 1 and 2 with renal progression in pathologically proven diabetic nephropathy (DN)...
August 24, 2017: Journal of Diabetes and its Complications
https://www.readbyqxmd.com/read/29032605/non-apoptotic-functions-of-fas-cd95-in-the-immune-response
#10
REVIEW
Jean-Philippe Guégan, Patrick Legembre
CD95 (also known as Fas) is a member of the tumor necrosis factor receptor (TNFR) superfamily. Its cognate ligand, CD95L, is implicated in immune homeostasis and immune surveillance. Mutations in this receptor are associated with a loss of apoptotic signaling and have been detected in an autoimmune disorder called autoimmune lymphoproliferative syndrome (ALPS) type Ia, which shares some clinical features with systemic lupus erythematosus (SLE). In addition, deletions and mutations of CD95 have been described in many cancers, which led researchers to initially classify this receptor as a tumor suppressor...
October 15, 2017: FEBS Journal
https://www.readbyqxmd.com/read/28993768/cd30-is-dispensable-for-t-cell-responses-to-influenza-virus-and-lymphocytic-choriomeningitis-virus-clone-13-but-contributes-to-age-associated-t-cell-expansion-in-mice
#11
Angela C Zhou, Laura M Snell, Michael E Wortzman, Tania H Watts
CD30 is a tumor necrosis factor receptor (TNFR) family member whose expression is associated with Hodgkin's disease, anaplastic large cell lymphomas, and other T and B lymphoproliferative disorders in humans. A limited number of studies have assessed the physiological role of CD30/CD30 ligand interactions in control of infection in mice. Here, we assess the role of CD30 in T-cell immunity to acute influenza and chronic lymphocytic choriomeningitis virus (LCMV) clone 13 infection, two viral infections in which other members of the TNFR superfamily are important for T-cell responses...
2017: Frontiers in Immunology
https://www.readbyqxmd.com/read/28990932/uromodulin-p-cys147trp-mutation-drives-kidney-disease-by-activating-er-stress-and-apoptosis
#12
Bryce G Johnson, Lan T Dang, Graham Marsh, Allie M Roach, Zebulon G Levine, Anthony Monti, Deepak Reyon, Lionel Feigenbaum, Jeremy S Duffield
Uromodulin-associated kidney disease (UAKD) is caused by mutations in the uromodulin (UMOD) gene that result in a misfolded form of UMOD protein, which is normally secreted by nephrons. In UAKD patients, mutant UMOD is poorly secreted and accumulates in the ER of distal kidney epithelium, but its role in disease progression is largely unknown. Here, we modeled UMOD accumulation in mice by expressing the murine equivalent of the human UMOD p.Cys148Trp point mutation (UmodC147W/+ mice). Like affected humans, these UmodC147W/+ mice developed spontaneous and progressive kidney disease with organ failure over 24 weeks...
October 9, 2017: Journal of Clinical Investigation
https://www.readbyqxmd.com/read/28969030/transmembrane-tnf-%C3%AE-promotes-activation-induced-cell-death-by-forward-and-reverse-signaling
#13
Meng Zhang, Jing Wang, Lingwei Jia, Jin Huang, Cheng He, Fuqing Hu, Lifei Yuan, Guihua Wang, Mingxia Yu, Zhuoya Li
Secretory tumor necrosis factor-alpha (sTNF-α) is known to mediate activation- induced cell death (AICD). However, the role of tmTNF-α in AICD is still obscure. Here, we demonstrated that tmTNF-α expression significantly increased accompanied with enhanced apoptosis during AICD in Jurkat and primary human T cells. Knockdown or enhancement of tmTNF-α expression in activated T cells suppressed or promoted AICD, respectively. Treatment of activated T cells with exogenous tmTNF-α significantly augmented AICD, indicating that tmTNF-α as an effector molecule mediates AICD...
September 8, 2017: Oncotarget
https://www.readbyqxmd.com/read/28965953/irhom2-deficiency-relieves-tnf-%C3%AE-associated-hepatic-dyslipidemia-in-long-term-pm2-5-exposed-mice
#14
Chen-Xu Ge, Yu-Ting Qin, De-Shuai Lou, Qiang Li, Yuan-Yuan Li, Zhong-Ming Wang, Wei-Wei Yang, Ming Wang, Nan Liu, Zhen Wang, Peng-Xing Zhang, Yan-Yang Tu, Jun Tan, Min-Xuan Xu
Accumulating researches reported that particulate matter (PM2.5) is a risk factor for developing various diseases, including metabolic syndrome. Recently, inactive rhomboid protein 2 (iRhom2) was considered as a necessary modulator for shedding of tumor necrosis factor-α (TNF-α) in immune cells. TNF-α, a major pro-inflammatory cytokine, was linked to various pathogenesis of diseases, including dyslipidemia. Here, wild type (WT) and iRhom2-knockout (iRhom2(-/-)) mice were used to investigate the effects of iRhom2 on PM2...
December 2, 2017: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/28934756/tumor-necrosis-factor-receptor-mediates-fibroblast-growth-factor-inducible-14-signaling
#15
REVIEW
Xuening Wang, Shengxiang Xiao, Yumin Xia
Tumor necrosis factor (TNF)-related weak inducer of apoptosis (TWEAK) engages its sole receptor, fibroblast growth factor-inducible 14 (Fn14), which participates in various inflammatory and immunologic processes. TWEAK/Fn14 interaction induces different cell fates depending on the local microenvironment, which correlates with certain expression profiles of TNF receptors (TNFR). The predominant expression of TNFR1 or TNFR2 facilitates cell death or proliferation, respectively, on TWEAK/Fn14 activation. TNFR-associated factors (TRAF) interact with Fn14, cellular inhibitor of apoptosis protein (cIAP)-1, and TNFR, consequently transducing signals from TWEAK to downstream cytokines and cell cycle mediators...
2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28926524/prognostic-significance-of-tnfr-associated-factor-1-and-2-traf1-and-traf2-in-glioblastoma
#16
Wenqing Zhang, Ying Sun, Lei Liu, Zongpeng Li
BACKGROUND TNFR-associated factor 1 (TRAF1) and TRAF2 have been demonstrated to inhibit apoptosis and promote cell survival in glioblastoma (GBM) cells with experiments in vitro. However, their clinical and prognostic significance have not been elucidated. MATERIAL AND METHODS In our study, we for the first time investigated the expression of TRAF1 and TRAF2 in 105 GBM tissues. Furthermore, we evaluated their clinical significance, including their association with clinicopathologic factors and prognostic value...
September 19, 2017: Medical Science Monitor: International Medical Journal of Experimental and Clinical Research
https://www.readbyqxmd.com/read/28912506/role-of-tumor-necrosis-factor-%C3%AE-and-its-receptors-in-diesel-exhaust-particle-induced-pulmonary-inflammation
#17
Smitha Kumar, Guy Joos, Louis Boon, Kurt Tournoy, Sharen Provoost, Tania Maes
Inhalation of diesel exhaust particles (DEP) induces an inflammatory reaction in the lung. However, the underlying mechanisms remain to be elucidated. Tumor necrosis factor alpha (TNF-α) is a pro-inflammatory cytokine that operates by binding to tumor necrosis factor receptor 1 (TNFR1) and tumor necrosis factor receptor 2 (TNFR2). The role of TNF-α signaling and the importance of either TNFR1 or TNFR2 in the DEP-induced inflammatory response has not yet been elucidated. TNF-α knockout (KO), TNFR1 KO, TNFR2 KO, TNFR1/TNFR2 double KO (TNFR-DKO) and wild type (WT) mice were intratracheally exposed to saline or DEP...
September 14, 2017: Scientific Reports
https://www.readbyqxmd.com/read/28877989/regulatory-t-cell-mediated-suppression-of-inflammation-induced-by-dr3-signaling-is-dependent-on-galectin-9
#18
Shravan Madireddi, So-Young Eun, Amit K Mehta, Aruna Birta, Dirk M Zajonc, Toshiro Niki, Mitsuomi Hirashima, Eckhard R Podack, Taylor H Schreiber, Michael Croft
Stimulation of several TNF receptor family proteins has been shown to dampen inflammatory disease in murine models through augmenting the number and/or activity of regulatory T cells (Tregs). We recently found that one molecule, 4-1BB, used binding to Galectin-9 to exert its immunosuppressive effects and drive expansion of CD8(+)Foxp3(-) Tregs. We now show that ligation of another TNFR family molecule, DR3, which has previously been found to strongly expand CD4(+)Foxp3(+) Tregs and suppress inflammation, also requires Galectin-9...
October 15, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/28875549/the-contribution-of-toll-like-receptor-signaling-to-the-development-of-liver-fibrosis-and-cancer-in-hepatocyte-specific-tak1-deleted-mice
#19
Isabelle Jingyi Song, Yoon Mee Yang, Sayaka Inokuchi-Shimizu, Yoon Seok Roh, Ling Yang, Ekihiro Seki
Hepatocyte death is associated with liver inflammation, fibrosis and hepatocellular carcinoma (HCC). Damaged cells trigger inflammation through activation of Toll-like receptors (TLRs). Although the role of TLR4 in HCC development has been reported, the role of TLR9 in the development of HCC remains elusive. To investigate the role of TLR4 and TLR9 signaling in liver inflammation-fibrosis-cancer axis, we took advantage of mice with hepatic deletion of transforming growth factor-β-activated kinase 1 (Tak1ΔHep) that develop spontaneous liver injury, inflammation, fibrosis, and HCC, recapitulating the pathology of human HCC...
September 5, 2017: International Journal of Cancer. Journal International du Cancer
https://www.readbyqxmd.com/read/28864474/the-scaffolding-protein-iqgap1-interacts-with-nlrc3-and-inhibits-type-i-ifn-production
#20
Aaron M Tocker, Emily Durocher, Kimberly D Jacob, Kate E Trieschman, Suzanna M Talento, Alma A Rechnitzer, David M Roberts, Beckley K Davis
Sensing of cytosolic nucleotides is a critical initial step in the elaboration of type I IFN. One of several upstream receptors, cyclic GMP-AMP synthase, binds to cytosolic DNA and generates dicyclic nucleotides that act as secondary messengers. These secondary messengers bind directly to stimulator of IFN genes (STING). STING recruits TNFR-associated NF-κB kinase-binding kinase 1 which acts as a critical node that allows for efficient activation of IFN regulatory factors to drive the antiviral transcriptome...
October 15, 2017: Journal of Immunology: Official Journal of the American Association of Immunologists
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