Tumour-necrosis factors articles within Nature Communications

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  • Article
    | Open Access

    MLKL is regarded as an executor of the necroptotic inflammatory cell death pathway. Here authors show, by introducing a mutation into mouse MLKL representing a frequently occurring human single nucleotide polymorphism, that MLKL mutations could critically alter the inflammatory response and the clearance of Salmonella from organs upon infection.

    • Sarah E. Garnish
    • , Katherine R. Martin
    •  & Joanne M. Hildebrand

  • Article
    | Open Access

    Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) is an important regulator of cell death pathways during embryogenesis and in infection/inflammation. Here authors show that tyrosine phosphorylation of RIPK1 by upstream kinases limits systemic inflammation and regulates haematopoietic homeostasis.

    • Hailin Tu
    • , Weihang Xiong
    •  & Xin Lin

  • Article
    | Open Access

    Reduction of systemic autoimmunity using TNF blockers may also reduce inflammatory diseases in other organs. Here, the authors use a patient database and scRNA-seq to link autoimmune diseases to benign prostatic hyperplasia (BPH), and demonstrate that prostatic hyperplasia is reduced by TNF blockers in humans and mice.

    • Renee E. Vickman
    • , LaTayia Aaron-Brooks
    •  & Simon W. Hayward

  • Article
    | Open Access

    Expansion of synovial fibroblast is associated with rheumatoid arthritis (RA) progression, but how this expansion is regulated is still not clear. Here the authors use a mouse RA model, single cell RNA sequencing and in vitro analyses to show that inducing ferroptosis and suppressing TNF signaling reduce fibroblast numbers and ameliorate experimental arthritis.

    • Jiao Wu
    • , Zhuan Feng
    •  & Ping Zhu

  • Article
    | Open Access

    Tumor necrosis factor (TNF) has various effects on phosphorylation-mediated cellular signaling. Combining phosphoproteomics, subcellular localization analyses and kinase inhibitor assays, the authors provide systems level insights into TNF signaling and identify modulators of TNF-induced cell death.

    • Maria C. Tanzer
    • , Isabell Bludau
    •  & Matthias Mann

  • Article
    | Open Access

    Controlled cell death can be an efficient anti-viral strategy, but also leads to tissue damage and needs to be balanced. Oyler-Yaniv et al. combine mathematical modelling and microscopy to show that exposure to TNF in response to viral infection causes cells to tune their speed-vs-accuracy trade-off in cell death decision to limit HSV-1 spread.

    • Jennifer Oyler-Yaniv
    • , Alon Oyler-Yaniv
    •  & Roy Wollman

  • Article
    | Open Access

    TNF can be inhibited by small molecules that stabilize the TNF trimer in an asymmetric conformation. Here, the authors develop a monoclonal antibody that selectively binds this inactive form of TNF, enabling both target engagement assessment and structural characterization of TNF binding to TNF receptor 1.

    • Daniel J. Lightwood
    • , Rebecca J. Munro
    •  & Alastair D. G. Lawson

  • Article
    | Open Access

    Small molecules stabilising a distorted TNF trimer can inhibit TNF signaling, but the underlying mechanism is unclear. Here, the authors characterize the inhibitor-bound TNF-receptor complex structurally and biochemically, showing that the inhibitors alter TNF-receptor binding stoichiometry and cluster formation.

    • David McMillan
    • , Carlos Martinez-Fleites
    •  & James O’Connell

  • Article
    | Open Access

    Altered monocyte responses and testosterone levels correlate, individually, with the pathogenesis of hepatic amebiasis in mice. Here the authors show that testosterone induces enhanced TNF/CXCL1 expression and stronger proinflammatory responses in both human and mouse monocytes to support an androgen-monocyte axis of inflammation regulation.

    • Julie Sellau
    • , Marie Groneberg
    •  & Hannelore Lotter

  • Article
    | Open Access

    Macrophage activation is tightly regulated to maintain immune homeostasis, yet activation is also heterogeneous. Here, the authors show that macrophages coordinate activation by partitioning into two phenotypes that can nonlinearly amplify collective inflammatory cytokine production as a function of cell density.

    • Joseph J. Muldoon
    • , Yishan Chuang
    •  & Joshua N. Leonard

  • Article
    | Open Access

    B cells contribute to rheumatoid arthritis pathogenesis and bone erosion, but the underlying mechanisms are still unclear. Here the authors show, using mouse models and patient tissues, that B cells directly inhibit osteoblast differentiation by producing CCL3 and TNF, thereby providing a potentially new direction for arthritis therapy.

    • Wen Sun
    • , Nida Meednu
    •  & Lianping Xing

  • Article
    | Open Access

    TNF mediated inflammation is critical in autoimmune mediated pathology, however many patients are refractory to current anti-TNF therapeutics. Here the authors show induction of several death ligands, in addition to TNF is sufficient to cause fatal dermatitis in a LUBAC deficient murine model of disease.

    • Lucia Taraborrelli
    • , Nieves Peltzer
    •  & Henning Walczak

  • Article
    | Open Access

    Lymphotoxin beta receptor (LTβR) signalling regulates leukocyte migration through the lymphatic endothelial layers. Here, the authors show that treatment of an LTβR-derived decoy peptide can target the non-classical NFκB pathway to inhibit T cell and dendritic cell migration and ameliorate contact hypersensitivity in mouse models.

    • Wenji Piao
    • , Yanbao Xiong
    •  & Jonathan S. Bromberg

  • Article
    | Open Access

    BAFF is an important cytokine for B cell survival, and is a therapeutic target for autoimmune disorders. Here the authors show that a 'flap' region of BAFF converts BAFFR binding events into survival signals and, with structural data, that this ‘flap’ differentially modulates binding of drugs such as belimumab or atacicept.

    • Michele Vigolo
    • , Melissa G. Chambers
    •  & Pascal Schneider

  • Article
    | Open Access

    The pathogenesis of paradoxical psoriasis in patients receiving anti-TNF treatments for classical psoriasis is unclear. Here, the authors show that anti-TNF drugs enhance the production of type I interferon by plasmacytoid dendritic cells, causing skin lesions that, unlike classical psoriasis, lack T- cell autoimmunity.

    • Curdin Conrad
    • , Jeremy Di Domizio
    •  & Michel Gilliet

  • Article
    | Open Access

    TWEAK is a TNF family member that binds the NFκB signalling receptor Fn14. Here the authors show that TWEAK is central to skin inflammation in mouse models of atopic dermatitis and psoriasis and causes similar pathology when injected subcutaneously into mice.

    • Daniel Sidler
    • , Ping Wu
    •  & Michael Croft

  • Article
    | Open Access

    Long-term consumption of a calorie-rich diet persistently activates brain microglia. Here, the authors show that microglial activity in mouse brains oscillates daily in conjunction with feeding, and that TNFα, secreted by activated microglia, induces mitochondrial stress in satiety-promoting POMC neurons.

    • Chun-Xia Yi
    • , Marc Walter
    •  & Matthias H. Tschöp

  • Article
    | Open Access

    Inflammatory cytokines such as TNF-α influence inflammation, apoptosis and tumour development through regulation of the kinase IKKβ. Krishnan and Nolte et al.apply quantitative proteomics to identify potential IKKβ targets, and reveal phosphorylation of AEG-1 by IKKβ as a mechanism controlling NF-κB signalling.

    • Ramesh K. Krishnan
    • , Hendrik Nolte
    •  & Jakub M. Swiercz

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