Interleukins articles within Nature Communications

Featured

  • Article
    | Open Access

    Deficiency in Wiskott-Aldrich syndrome protein (WASP) has been associated with autoimmune colitis, but the underlying mechanism is still unclear. Here the authors show that WASP deficiency is associated with defective WASP/DOCK8 complex formation, altered IL-10 signalling, and impaired anti-inflammatory macrophage functions.

    • Amlan Biswas
    • , Dror S. Shouval
    •  & Scott B. Snapper

  • Article
    | Open Access

    Systemic lupus erythematosus (SLE) is associated with altered B cell responses but the underlying aetiology is still unclear. Here the authors show that a CD11chiT-bet+ B cell subset with a unique phenotype and transcriptome is increased in patients with SLE, can be expanded by IL-21, and may contribute to autoimmune responses in SLE.

    • Shu Wang
    • , Jingya Wang
    •  & Rachel Ettinger

  • Article
    | Open Access

    Inflammation can be induced by obesity, and has been linked with onset of colorectal cancer (CAC). Here the authors show in mouse models that obesity-induced interleukin-6 alters macrophage function to enhance CCL-20/CCR-6-mediated recruitment of B cells and γδ T cells, thereby promoting gut inflammation and CAC progression.

    • Claudia M. Wunderlich
    • , P. Justus Ackermann
    •  & F. Thomas Wunderlich

  • Article
    | Open Access

    The IL-1 evolutionary history is essential in our understanding of function and development. Here the authors use molecular phylogenetic analysis to probe the IL-1 family in a range of species, suggesting disparate phylogenetic association of IL-18 and IL-33 proteins within the IL-1 family.

    • Jack Rivers-Auty
    • , Michael J. D. Daniels
    •  & David Brough

  • Article
    | Open Access

    Semaphorin-4A is a cell surface protein with known functions in neural development and immune regulation, but the mechanism for immune modulation is unclear. Here the authors show that ILT-4, previously found on myeloid cells, is the receptor of Semaphorin-4A on activate human CD4 T cells for mediating T cell co-stimulation.

    • Ning Lu
    • , Ying Li
    •  & Lieping Chen

  • Article
    | Open Access

    The N-terminal domain (NTD) of interleukin-3 receptor α-subunit (IL3Rα) is involved in IL-3 recognition but the underlying mechanism is unknown. Here, the authors present crystal structures of the IL3Rα complex and provide biochemical evidence that the NTD regulates IL-3 binding and signalling complex assembly.

    • Sophie E. Broughton
    • , Timothy R. Hercus
    •  & Michael W. Parker

  • Article
    | Open Access

    B cells are important for antigen presentation and antibody production in humoral immunity, but are also increasingly recognized for their immune regulatory functions. Here the authors show that HIF-1α, a hypoxia-induced transcription factor, is important for controlling IL-10 induction in and immune-suppressive activity of B cells.

    • Xianyi Meng
    • , Bettina Grötsch
    •  & Aline Bozec

  • Article
    | Open Access

    High dose IL-2 is a viable treatment option for cancer immune therapy, but the underlying mechanism for the accompanying undesirable morbidity is unclear. Here the authors show, using human immune system mouse models, that regulatory T cells and their functions on effector T cells are essential modulators of the related pathogenesis.

    • Yan Li
    • , Helene Strick-Marchand
    •  & James P. Di Santo

  • Article
    | Open Access

    T cells help B cells to differentiate into antibody-producing plasma cells. Here the authors show that T cells produce interleukin-2 to activate ERK/ELK1 and suppress BACH2 expression by modulating the BACH2 super-enhancer, thereby altering BACH2 downstream transcription programs for plasma cell differentiation.

    • Nicolas Hipp
    • , Hannah Symington
    •  & Céline Delaloy

  • Article
    | Open Access

    Neutrophils are important modulators of tissue damage after intracerebral hemorrhage (ICH), but how this function is regulated is not clear. Here, the authors show interleukin-27 promotes the tissue-protecting functions of neutrophils via, at least partly, the induction of lactoferrin to present a potential therapy for ICH.

    • Xiurong Zhao
    • , Shun-Ming Ting
    •  & Jaroslaw Aronowski

  • Article
    | Open Access

    NOTCH signalling stimulates oligodendrocyte progenitor cell proliferation but how this regulates demyelinating disease is unclear. Here, the authors show that an IL-17 adaptor protein, Act1, interacts with the C-terminal fragment of NOTCH1 (NICD) to activate cell proliferation and an inflammatory response.

    • Chenhui Wang
    • , Cun-Jin Zhang
    •  & Xiaoxia Li

  • Article
    | Open Access

    How NALP7 inflammasome formation is regulated is unclear. Here the authors show that STAMBP prevents lysosomal degradation of NALP7 and present BC-1471 as a potential therapeutic STAMBP inhibitor, showing it can reduce TLR-induced IL-1β production.

    • Joseph S. Bednash
    • , Nathaniel Weathington
    •  & Rama K. Mallampalli

  • Article
    | Open Access

    Interleukin-6 (IL-6) is increased in obesity and activates T cells to promote inflammation. Here, Xuet al. use mice that lack IL-6 receptors on T cells to uncover the temporal and tissue-specific effects of classic and trans IL-6 signalling on inflammation and insulin resistance on a high-fat diet.

    • Elaine Xu
    • , Mafalda M. A. Pereira
    •  & Jens C. Brüning

  • Article
    | Open Access

    ILC2 and ILC3 are generally thought to require IL-7. Here the authors use IL-7 ko mice and provide side-by-side comparison of ILCs from different tissues to show that IL-7 signalling is not required for intestinal ILC maintenance or function and that IL-15 can compensate for absence of IL-7.

    • Michelle L. Robinette
    • , Jennifer K. Bando
    •  & Marco Colonna

  • Article
    | Open Access

    Cytokines and their associated pathways can affect survival ofMycobacterium tuberculosis in macrophages, representing potential targets for host-directed therapies. Here, Péan et al. show that cytokine-STAT signalling promotes mycobacterial survival within macrophages by deregulating lipid droplet homeostasis.

    • Claire B. Péan
    • , Mark Schiebler
    •  & Marc S. Dionne

  • Article
    | Open Access

    In patients with cystic fibrosis, IL-9 signalling is increased. The authors describe an inflammatory loop in which IL-9 produced by Th9 cells drives mast cells to produce IL-2, resulting in ILC2 cell activation, and show inhibition of this loop with blocking antibodies to IL-9 in a mouse model of pulmonary infection.

    • Silvia Moretti
    • , Giorgia Renga
    •  & Luigina Romani

  • Article
    | Open Access

    IL-12 and IL-23 share the common p40 subunit yet have distinct immunological functions with IL-12 typically contributing to Th1 responses and IL-23 to Th17 responses. Here the authors show that current p40 based therapies for psoriasis are counterproductive owing to an IFN-γ-independent tissue protective function of IL-12 in skin.

    • Paulina Kulig
    • , Stephanie Musiol
    •  & Burkhard Becher

  • Article
    | Open Access

    Ventricular arrhythmia is a leading cause of death in patients with diabetes. Here the authors show that inflammasome activation and ILK-1β production in cardiac macrophages cause arrhythmia in diabetic mice, which can be successfully treated using agonists to IL-1β receptor or NLRP3 inhibitors.

    • Gustavo Monnerat
    • , Micaela L. Alarcón
    •  & Emiliano Medei

  • Article
    | Open Access

    Tiam1 is a guanine nucleotide exchange factor for the Rho-family GTPase Rac1. Here, the authors show that nuclear Tiam1 and Rac1 bind to RORγt on the IL-17 promoter, activating its transcription, and that inhibiting Tiam1/Rac1 is beneficial in a mouse model of autoimmunity.

    • Ahmed T. Kurdi
    • , Ribal Bassil
    •  & Wassim Elyaman

  • Article
    | Open Access

    Type 1 diabetes is driven by T-cell autoimmunity to pancreatic islet cells. Here the authors show that autoreactive anti-IL-2 T and B cells are present in type 1 diabetes patients, and that anti-IL-2 antibodies precede diabetes onset in mice, suggesting their potential as a diagnostic marker.

    • Louis Pérol
    • , John M. Lindner
    •  & Eliane Piaggio

  • Article
    | Open Access

    High-affinity IL-2Rα expressed by Tregs mitigates the potential of IL-2 use in cancer therapy. Here, the authors fuse IL-2 with an NKDG2 binding domain, and show that it induces IL-2 signalling selectively in NKG2D+cells, delaying tumour growth in mice without the side effects of conventional IL-2 therapy.

    • Reza Ghasemi
    • , Eric Lazear
    •  & Alexander Sasha Krupnick

  • Article
    | Open Access

    Chitinase 3-like 1 regulates cell death, inflammation and tissue remodelling via IL-13receptorα2. Here, the authors show that TMEM219 is a IL-13Rα2 co-receptor and modulates oxidant-induced apoptosis and lung injury, melanoma metastasis and TGF-β1 signalling, downstream of Chi3l1-IL-13Rα2.

    • Chang-Min Lee
    • , Chuan Hua He
    •  & Jack A. Elias

  • Article
    | Open Access

    Epidermal intraepithelial lymphocytes (IEL) produce IL-13, but the physiological role of this cytokine production is not clear. Here the authors show that IEL-production of IL-13 is a vital lymphoid stress surveillance mechanism driving crosstalk with epithelial cells to maintain tissue homeostasis and inhibit chemical carcinogenesis in mice.

    • Tim Dalessandri
    • , Greg Crawford
    •  & Jessica Strid

  • Article
    | Open Access

    Transcription factors directing T cell fate are induced by instructive signals such as cytokines. Here the authors show that IL-15 promotes Foxp3 and inhibits RORγt expression in CD4 T cells, and that IL-15 is critical to suppress colitis by maintaining the Treg to Th1/Th17 ratio in a mouse model.

    • Milena J. Tosiek
    • , Laurence Fiette
    •  & Antonio A. Freitas

  • Article
    | Open Access

    γδ T cells are innate-like lymphocytes that regulate immune responses by producing IL-17A or IFN-γ, but have no known role in bone healing. Here the authors show a nonimmune bone-regenerative function of IL-17A produced by the Vγ6+ subset in mice.

    • Takehito Ono
    • , Kazuo Okamoto
    •  & Hiroshi Takayanagi

  • Article
    | Open Access

    It remains incompletely understood how cytokines shape TH1 cell differentiation to central memory T (TCM) and follicular T helper (TFH) cells. Here the authors show that TH1 cells can co-initiate the expression of both TFH and TCM gene programs and that IL-7 signalling represses TFH-associated but not TCM-associated genes.

    • Paul W. McDonald
    • , Kaitlin A. Read
    •  & Kenneth J. Oestreich

  • Article
    | Open Access

    IL-33, released by epithelial cells in response to stress, is a potent activator of inflammation. Here Cohenet al. show that secreted IL-33 is rapidly inactivated by disulfide bond formation that prevents binding to its receptor, and that IL-33-related cytokines are susceptible to similar oxidation.

    • E. Suzanne Cohen
    • , Ian C. Scott
    •  & Tomas Mustelin

  • Article
    | Open Access

    T follicular helper cells are a distinct subtype of CD4 T helper cells, which contributes to the regulation of type 2 humoral immunity by producing IL-4. Here, the authors identify Batf as an important transcription factor regulating IL-4 expression in T follicular helper cells but not in Th2 cells.

    • Anupama Sahoo
    • , Andrei Alekseev
    •  & Roza Nurieva

  • Article
    | Open Access

    HIV-infected patients who maintain undetectable virus levels possess elevated plasma concentrations of IL-21. Here, Adoroet al. show that IL-21 inhibits early viral infection in humanized mice and suppresses HIV-1 replication in vitroby upregulating a microRNA via the regulatory protein STAT3.

    • Stanley Adoro
    • , Juan R. Cubillos-Ruiz
    •  & Laurie H. Glimcher

  • Article
    | Open Access

    Control of γδ T-cell activation remains incompletely understood. Here the authors show that during autoimmune arthritis development αβ CD4+T cells recruit a subset of IL-17-producing γδ T cells to the joints, and that both components are essential to cause pathology in a mouse model of the disease.

    • Aoi Akitsu
    • , Harumichi Ishigame
    •  & Yoichiro Iwakura

  • Article
    | Open Access

    Macrophages activate gene expression of alternative activation program in response to IL-13. Here the authors show that Liver Receptor Homologue-1 regulates synthesis of lipid metabolites stimulating antifungal and repressing proinflammatory genes in macrophages exposed to IL-13 through PPAR activation.

    • Lise Lefèvre
    • , Hélène Authier
    •  & Agnès Coste

  • Article
    | Open Access

    Collagen 3 is increased during tendon repair, but is then replaced by Collagen 1 that has superior biomechanical properties. Here the authors show that IL-33 is induced by tendon damage and regulates miR-29a, which controls Collagen 3 production and feeds back on IL-33, orchestrating tendon repair.

    • Neal L. Millar
    • , Derek S. Gilchrist
    •  & Iain B. McInnes

Browse broader subjects

Browse Interleukins across other nature.com journals