Immunological disorders articles within Nature Communications

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  • Article
    | Open Access

    Neuromyelitis optica (NMO) is a rare autoimmune condition characterized by inflammation and demyelination of the optic nerve and the spinal cord. Here, Estrada et al. identify NMO susceptibility variants in the MHC region and find that autoantibody-positive NMO genetically overlaps with lupus.

    • Karol Estrada
    • , Christopher W. Whelan
    •  & Daniel G. MacArthur

  • Article
    | Open Access

    Allergen-specific immunotherapy is used to treat patients affected by acute immunoglobulin E (IgE) responses, but the function mechanism is unclear. Here the authors show that the administration of two cat allergen-specific IgGs reduces allergic responses in mouse models and helps ameliorate clinical symptoms in a phase 1b clinical trial.

    • J. M. Orengo
    • , A. R. Radin
    •  & G. D. Yancopoulos

  • Article
    | Open Access

    Matrix metalloproteinases (MMP) are involved in vascular remodeling associated with plaque progression. Little is known about their immune regulatory role in vascular disorders. Here, the authors report that MT4-MMP-deficiency increases the recruitment of patrolling monocytes to early atherosclerotic lesions, which accelerates atherosclerosis.

    • Cristina Clemente
    • , Cristina Rius
    •  & Alicia G. Arroyo

  • Article
    | Open Access

    XLP-2 syndrome is caused by XIAP mutation. Here the authors show that mouse and human XIAP-deficient regulatory T cells have defective suppressive function as a result of conversion to proinflammatory cytokine producing cells, an effect that can be prevented by blocking the IL-6 receptor.

    • Wan-Chen Hsieh
    • , Tzu-Sheng Hsu
    •  & Ming-Zong Lai

  • Article
    | Open Access

    Post-translational modifications are associated with autoimmune diseases but definitive evidence of their contribution to escape from central tolerance mechanisms is needed. Here, the authors show that T cells specific for post-translational modifications of type II collagen escape intrathymic tolerance induction in a mouse model of rheumatoid arthritis.

    • Bruno Raposo
    • , Patrick Merky
    •  & Johan Bäcklund

  • Article
    | Open Access

    Clinical trials of BAFF blockade with belimumab have shown partial efficacy for the treatment of systemic lupus erythematosus (SLE), so other therapeutic options are required. Here, the authors present a new small molecule inhibitor that targets NIK with a similar efficacy to BAFF inhibition in two mouse models of SLE.

    • Hans D. Brightbill
    • , Eric Suto
    •  & Nico Ghilardi

  • Article
    | Open Access

    Colonization of commensal bacteria is thought to impact immune development, especially in the earliest years of life. Here, the authors show, by analyzing the development of the gut microbiome of 690 children, that microbial composition at the age of 1 year is associated with asthma diagnosed in the first 5 years of life.

    • Jakob Stokholm
    • , Martin J. Blaser
    •  & Hans Bisgaard

  • 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

    IgE is linked to allergic diseases and there is a great interest in developing anti-IgE therapeutics. Here the authors characterize the binding of human IgE Fc to a single domain antibody (sdab) and show that the sdab induces a closed conformation, which prevents and disrupts IgE binding to its receptor FcεRI and abrogates allergen mediated activation.

    • Frederic Jabs
    • , Melanie Plum
    •  & Edzard Spillner

  • Article
    | Open Access

    Nucleic acid sensing is important to ensure that an innate immune response is only mounted against microbial nucleic acid. Here, the authors identify loss-of-function mutations in the DNASE2 gene that cause type I interferon-mediated autoinflammation due to enhanced systemic interferon signaling.

    • Mathieu P. Rodero
    • , Alessandra Tesser
    •  & Yanick J. Crow

  • Article
    | Open Access

    The NLRP3 inflammasome is central to a variety of inflammatory diseases, but how it is regulated to prevent excessive inflammation is not clear. Here the authors show that NLRP3 activation causes SHP2 translocation to the mitochondria to interact with and dephosphorylate ANT1, thus stabilizing the mitochondria and preventing release of proinflammatory mitochondrial DNA and ROS.

    • Wenjie Guo
    • , Wen Liu
    •  & Qiang Xu

  • Article
    | Open Access

    Rising rates of peanut allergy pose a public health problem. Here, the authors profile blood transcriptomes during double-blind, placebo-controlled oral challenge in peanut-allergic children to identify gene and cell composition changes, and construct causal networks to detect key allergic reaction drivers.

    • C. T. Watson
    • , A. T. Cohain
    •  & S. Bunyavanich

  • Article
    | Open Access

    Complement component C1q activates efferocytosis, suppresses inflammatory responses, and is thereby thought to limit autoimmune disease. Here, the authors show that macrophage transcription factor MafB regulates total serum levels of C1q, which contributes to preventing autoimmune disease in mice.

    • Mai Thi Nhu Tran
    • , Michito Hamada
    •  & Satoru Takahashi

  • Article
    | Open Access

    Wiskott-Aldrich syndrome protein (WASp) is essential for controlling the cytoskeleton, but its function in innate immunity is unclear. Here the authors show that WASp deficiency is associated with dysregulated septin cage formation, excessive inflammasome activation, elevated immune cell death and reduced bacterial clearance.

    • Pamela P. Lee
    • , Damián Lobato-Márquez
    •  & Adrian J. Thrasher

  • Article
    | Open Access

    IgE is an important mediator of protective immunity as well as allergic reaction, but how high affinity IgE antibodies are produced in memory responses is not clear. Here the authors show that IgE can be generated via class-switch recombination in IgG1 memory B cells without additional somatic hypermutation.

    • Jin-Shu He
    • , Sharrada Subramaniam
    •  & Maria A. Curotto de Lafaille

  • Article
    | Open Access

    Non-invasive cell tracking is a powerful method to visualize cells in vivo under physiological and pathophysiological conditions. Here Thunemann et al. generate a mouse model for in vivo tracking and quantification of specific cell types by combining a PET reporter gene with Cre-dependent activation that can be exploited for any cell population for which a Cre mouse line is available.

    • Martin Thunemann
    • , Barbara F. Schörg
    •  & Robert Feil

  • Article
    | Open Access

    Graft-vs.-host disease is a complication of allogenic hematopoietic stem cell transplantation, and is associated with endothelial dysfunction. Here the authors show that activated protein C signals via PAR2/PAR3 to expand Treg cells, mitigating the disease in mice.

    • Satish Ranjan
    • , Alexander Goihl
    •  & Berend Isermann

  • Article
    | Open Access

    Systemic lupus erythematosus (SLE) is an autoimmune disease with a strong ethnic and gender bias. In a transancestral genetic association study, Langefeldet al. identify 24 novel regions associated with risk to lupus and propose a cumulative hits hypothesis for loci conferring risk to SLE.

    • Carl D. Langefeld
    • , Hannah C. Ainsworth
    •  & Timothy J. Vyse

  • Article
    | Open Access

    Axl is a TAM receptor that can inhibit Toll-like receptor (TLR) -induced pro-inflammatory production by dendritic cells (DC). Here the authors show that miR-34a targets Axl to control CD1c+ DC activity in mice, and that miR-34a-deficient mice are resistant to collagen-induced arthritis, whereas DCs from patients with rheumatoid arthritis have high levels of miR- 34a.

    • Mariola Kurowska-Stolarska
    • , Stefano Alivernini
    •  & Iain B. McInnes

  • 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

    ARPC1B is a component of the actin-related protein 2/3 complex (Arp2/3), which is required for actin filament branching. Kahret al. show that ARPC1B deficiency in humans is associated with severe multisystem disease that includes platelet abnormalities, eosinophilia, eczema and other indicators of immune disease.

    • Walter H. A. Kahr
    • , Fred G. Pluthero
    •  & Aleixo M Muise

  • Article
    | Open Access

    CARMIL2 (Rltpr) is involved in T-cell function. Here, the authors identify human CARMIL2-deficiency as an autosomal recessive primary immunodeficiency disorder characterized by EBV+smooth muscle tumours, CD28 co-signalling deficiency and impaired cytoskeletal dynamics.

    • T. Schober
    • , T. Magg
    •  & F. Hauck

  • Article
    | Open Access

    Germinal centre (GC) reactions are driven by T follicular helper (Tfh) cells and their dysregulation can cause autoimmune disease. Here the authors show that the orphan receptor DR6 is a Tfh cell marker that binds syndecan-1 on GC B cells driving autoimmunity in lupus-prone mice.

    • Daisuke Fujikura
    • , Masahiro Ikesue
    •  & Toshimitsu Uede

  • Article
    | Open Access

    JAK1 mediates intracellular signalling from multiple cytokine receptors. Here, Elettoet al. identify JAK1 mutations that disrupt multiple signalling pathways and are associated with primary immunodeficiency, atypical mycobacterial infection susceptibility and early-onset metastatic bladder carcinoma.

    • Davide Eletto
    • , Siobhan O. Burns
    •  & Sergey Nejentsev

  • 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

    Angiopoietin-like 4 protein (ANGPTL4) is a regulator of lipoprotein metabolism whose role in atherosclerosis has been controversial. Here the authors show that ANGPTL4 deficiency in haematopoietic cells increases atherogenesis by promoting myeloid progenitor cell expansion and differentiation, foam cell formation and vascular inflammation.

    • Binod Aryal
    • , Noemi Rotllan
    •  & Carlos Fernández-Hernando

  • Article
    | Open Access

    Hrd1 is an E3 ubiquitin ligase involved in ER-associated degradation and MHC I turnover. Here the authors use T-cell-specific ko mice and a mouse model of multiple sclerosis to show that Hrd1 also drives pro-inflammatory T helper cell responses and contributes to pathogenesis of autoimmune disease.

    • Yuanming Xu
    • , Fang Zhao
    •  & Deyu Fang

  • Article
    | Open Access

    Evidence of how functional Bregs develop in vivo has been lacking. Here the authors show that proB cells exposed in vivoto CpG differentiate into distinct Breg subsets that inhibit autoimmunity by arresting T cells in the lymph nodes via CCL19 and by producing IL-10 at the site of immunopathology.

    • Sarantis Korniotis
    • , Christophe Gras
    •  & Flora Zavala

  • Article
    | Open Access

    The gut microbiome has been implicated in several autoimmune disorders. Here, the authors study the gut microbiome of patients with multiple sclerosis, and find correlations between altered abundance of certain gut microorganisms and changes in expression of immune defence genes.

    • Sushrut Jangi
    • , Roopali Gandhi
    •  & Howard L. Weiner

  • Article
    | Open Access

    Endothelial to mesenchymal transition (EndMT) is a crucial developmental process that also plays a role in the pathogenesis of some diseases. Here the authors show that EndMT contributes to the development of atherosclerosis in mice and humans, and is associated with complex human plaques that may be prone to rupture.

    • Solene M. Evrard
    • , Laura Lecce
    •  & Jason C. Kovacic

  • Article
    | Open Access

    STING is essential for the type I interferon immune response to foreign DNA. Here, the authors show that palmitoylation of STING at the Golgi is required for activating downstream signalling, and increased Golgi localization of certain STING variants may cause autoimmune disease in some cases.

    • Kojiro Mukai
    • , Hiroyasu Konno
    •  & Tomohiko Taguchi

  • Article
    | Open Access

    Rheumatoid arthritis is an inflammatory disease that selectively affects different joints. Here the authors show that gene expression and DNA methylation patterns of fibroblast-like synoviocytes differ between hip and knee joints in patients with RA, thus providing epigenetic and transcriptomic evidence for this anatomic selectivity of inflammation.

    • Rizi Ai
    • , Deepa Hammaker
    •  & Wei Wang

  • Article
    | Open Access

    Here, Dirk Lefeber and colleagues identify functional mutations in ATP6AP1 encoding Ac45. The authors show that Ac45 is the functional ortholog of yeast V-ATPase assembly factor Voa1 and provide evidence for tissue-specific Ac45 processing, associated with the clinical phenotype of immunodeficiency, hepatopathy, and neurocognitive abnormalities.

    • Eric J. R. Jansen
    • , Sharita Timal
    •  & Dirk J. Lefeber

  • Article
    | Open Access

    Experimental autoimmune encephalomyelitis (EAE) involves inflammatory cell infiltration into the central nervous system (CNS) and models the human disease multiple sclerosis. Here the authors show that transferred CD4+ gut intraepithelial lymphocytes can migrate into the CNS and inhibit inflammation in recipient mice with EAE.

    • Atsushi Kadowaki
    • , Sachiko Miyake
    •  & Takashi Yamamura

  • Article
    | Open Access

    How transcription factor T-bet and Th17 cells contribute to colitis remains incompletely understood. Here the authors identify T-bet as a negative regulator of IL-23R pathway activation and show that T-bet deficient T cells drive colitogenic Th17 responses dependent on the cytokines IL-17A and IL-22.

    • Thomas Krausgruber
    • , Chris Schiering
    •  & Fiona Powrie

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