Immunological disorders articles within Nature Communications

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  • Article
    | Open Access

    Faecal microbiota transplantation (FMT) can be used to treat established colitis. Here the authors profile transcriptional changes in humans after FMT and how this relates to colitis remission identifying a role for GBP5, and this protein is validated in a loss-of-function mouse model.

    • Laurence D. W. Luu
    • , Abhimanu Pandey
    •  & Nadeem O. Kaakoush

  • Article
    | Open Access

    IgG4-related disease is a fibro-inflammatory disorder, characterized by infiltration of IgG4 producing plasma cells in the target organs. Here authors show that the affected B cells express less ubiquitin-specific protease 25 (USP25), and this results in activation of multiple pathways involved in cytoskeleton reorganization, inflammation and energy metabolism, which might govern disease pathogenesis.

    • Panpan Jiang
    • , Yukai Jing
    •  & Chaohong Liu

  • Article
    | Open Access

    Regulation of thymocyte development by RNA-binding proteins is not fully characterized. Here the authors show the RBP ARPP21 interacting with the Rag1 3’-UTR to promote Rag1 expression, TCR rearrangement and an increased diversity of the TCR repertoire and that ARPP21 is down regulated by TCR stimulation.

    • Meng Xu
    • , Taku Ito-Kureha
    •  & Vigo Heissmeyer

  • Article
    | Open Access

    Cytidine nucleotide triphosphate (CTP) is a key precursor involved in the metabolism of DNA, RNA and phospholipids. In this study, the authors examine the physiological consequences of CTP synthase (Ctps) 1 and 2 deletion in vivo and demonstrate that Ctps1 protects mice from fatal autoimmunity.

    • Claire Soudais
    • , Romane Schaus
    •  & Sylvain Latour

  • Article
    | Open Access

    Classical monocytes can differentiate into pro-inflammatory or pro-resolving macrophages. Here the authors characterise mouse macrophage differentiation and show that Ly6Chi classical monocytes can differentiate into Ly6Clo pro-resolving macrophages which are involved in the resolution of skin allergic inflammation.

    • Kensuke Miyake
    • , Junya Ito
    •  & Hajime Karasuyama

  • Article
    | Open Access

    Gain-of-function mutations in NLRP3 result in Cryopyrin-Associated Periodic Syndrome in human patients. Here authors show that although these NLRP3 variants are constitutively active, they preserve their responsiveness to external pro-inflammatory stimuli, and they interfere with the immune-metabolic inflammatory pathways in monocytes.

    • Cristina Molina-López
    • , Laura Hurtado-Navarro
    •  & Pablo Pelegrin

  • Article
    | Open Access

    The clinical success of anti- αEβ7 antibody Etrolizumab for Crohn’s disease is less than what is expected based on proof-of-concept studies. Here authors show, by characterization of T cells from Etrolizumab-treated patients, in vitro functional assays and reanalysis of public single cell datasets on Etrolizumab-treated patients, that at high level of T cell activation, which characterises T cells in Crohn’s disease, E-Cadherin-αEβ7 interactions become resistant to Etrolizumab inhibition.

    • Maximilian Wiendl
    • , Mark Dedden
    •  & Sebastian Zundler

  • Article
    | Open Access

    Acquired mutations of the gene UBA1 occurring in myeloid cells that result in the expression of impaired isoforms of the enzyme E1 have been described in patients with a severe adult onset auto-inflammatory syndrome called VEXAS. Here the authors profile patients with UBA1 mutations presenting with or without VEXAS disease and show VEXAS disease is characterized by inflammasome activation and monocyte dysregulation.

    • Olivier Kosmider
    • , Céline Possémé
    •  & Benjamin Terrier

  • Article
    | Open Access

    Fibroblast heterogeneity is a recognized feature in chronic kidney disease, and although fibrosis is integrant to the pathology, it is lesser known which of the fibroblast populations contribute. Here authors describe a population of proinflammatory fibroblasts, which are found in close proximity to macrophages and may facilitate their recruitment and acquisition of a FOLR2+, pathogenic phenotype.

    • Camille Cohen
    • , Rana Mhaidly
    •  & Fatima Mechta-Grigoriou

  • Article
    | Open Access

    Steroid-refractory acute graft-versus-host disease (aGVHD) is associated with a low one-year survival rate. Here, the authors show that ROCK1 is upregulated in leukocytes from patients with steroid-refractory aGVHD and that ROCK1/2 inhibition reduces the severity of aGVHD in mice by interfering with activation of multiple immune cell types.

    • Kristina Maas-Bauer
    • , Anna-Verena Stell
    •  & Robert Zeiser

  • Article
    | Open Access

    Apoptotic and lytic cell death pathways are both utilised in the removal of damaged cells; however, the downstream inflammatory outcomes widely vary according to the chosen pathway. Here authors show that in mice with genetic deletion of Gasdermin E specifically in neutrophils, these cells undergo apoptosis rather than pyroptotic cell death upon senescence, with consequential attenuation of reactive inflammatory responses.

    • Fengxia Ma
    • , Laxman Ghimire
    •  & Hongbo R. Luo

  • Article
    | Open Access

    Mast cells have been shown to be involved with rheumatoid arthritis, but the mechanisms are not clear. Here using mouse models and making association with human patients, the authors show mast cells have an important function in the pathogenesis of rheumatoid arthritis, involving regulation of T cell responses and release of mast cell mediators.

    • Yunxuan Lei
    • , Xin Guo
    •  & Guangjie Chen

  • Article
    | Open Access

    IgA protects mucosal barriers by coating microorganisms, yet infection related complications are rare in human IgA deficiency. Authors here show that in humans lacking IgA, IgG assists IgM in coating of most bacterial families, thus contributing to gut mucosal defence.

    • Carsten Eriksen
    • , Janne Marie Moll
    •  & Susanne Brix

  • Article
    | Open Access

    Acute GVHD severity grading is based on target organ assessments. Here, the authors show that data-driven grading can identify 12 distinct grades with specific aGVHD phenotypes, which are associated with clinical outcomes, and that their method outperformed conventional gradings.

    • Evren Bayraktar
    • , Theresa Graf
    •  & Amin T. Turki

  • Article
    | Open Access

    Type-1 diabetes pathogenesis has been strongly linked with changes in the intestinal microbiota. Here, the authors demonstrate that mice susceptible to type-1 diabetes become resistant when co-housed with resistant mice, an effect that was associated with changes in gut microbiota, gut permeability, and the immune system.

    • Estela Rosell-Mases
    • , Alba Santiago
    •  & Chaysavanh Manichanh

  • Article
    | Open Access

    Although B cell-targeting therapies can provide clinical benefits to children with idiopathic nephrotic syndrome (INS), B lymphocyte subsets have not been extensively studied in this disease. Here, using single-cell RNA sequencing, the authors identify an extrafollicular B cell signature in children with INS.

    • Tho-Alfakar Al-Aubodah
    • , Lamine Aoudjit
    •  & Tomoko Takano

  • Article
    | Open Access

    Although type-1 diabetes has a clear genetic component, not all children who are at risk eventually develop autoimmunity, suggesting the existence of environmental triggers. In this longitudinal transcriptomic study, the authors find that children who later develop autoimmunity have a distinct profile before the appearance of autoantibodies and may have impaired responses to enterovirus infection.

    • Jake Lin
    • , Elaheh Moradi
    •  & Matti Nykter

  • Article
    | Open Access

    B cell clonal expansion and affinity maturation takes place in germinal centers (GC) and is orchestrated by follicular T cells. Here authors show that naïve conventional T cells are continuously recruited to the GCs during the GC reaction and develop into follicular helper and regulatory T cells, thus quantitatively contribute to remodelling the GC overtime.

    • Julia Merkenschlager
    • , Riza-Maria Berz
    •  & Michel C. Nussenzweig

  • Article
    | Open Access

    Psoriasis is a common inflammatory disease, and the overproduction of reactive oxygen species (ROS) in skin lesions plays a critical role in the progress of psoriasis. Here, the authors report the use of multienzyme-inspired biomimetic iron single-atom catalysts (FeN4O2-SACs) with broad-spectrum ROS-scavenging capability for psoriasis treatment and relapse prevention via related gene restoration.

    • Xiangyu Lu
    • , Le Kuai
    •  & Jianlin Shi

  • Article
    | Open Access

    Autoimmune vasculitis can be heterogeneous in terms of immune cell involvement. Here the authors use a single cell transcriptomics approach to characterise a group of microscopic polyangiitis patients that could be split into two groups typified by monocyte or Interferon associated gene expression.

    • Masayuki Nishide
    • , Kei Nishimura
    •  & Atsushi Kumanogoh

  • Article
    | Open Access

    Psoriasis is a chronic, systemic inflammatory condition primarily affecting skin. Here, the authors investigate the genetic basis of gene expression in skin biopsies from psoriasis patients and interactions with inflammation to better understand mechanisms of the disease.

    • Qian Xiao
    • , Joseph Mears
    •  & Soumya Raychaudhuri

  • Article
    | Open Access

    Atopic dermatitis is an inflammatory skin disease featuring systemic involvement. Here authors show that the two major clinical manifestations of the disease, erythema and papulation, are distinguished by differential interplay between local skin and systemic immunity, uncovered by integrated transcriptomics.

    • Aiko Sekita
    • , Hiroshi Kawasaki
    •  & Haruhiko Koseki

  • 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

    The regulation and intracellular transport of Ca2+ in immune cells involves Ca2+ release-activated Ca2+ (CRAC) channels. Here the authors show targeting CRAC components Orai1 and Orai2 modulates pulmonary ILC2 cells altering their metabolism, function and is linked to alleviation of immunopathology in a murine model of allergic airway disease.

    • Emily Howard
    • , Benjamin P. Hurrell
    •  & Omid Akbari

  • Article
    | Open Access

    The mechanistic functions of neutrophils in skin inflammation are not fully understood. Here the authors use human psoriasis samples and a mouse model of skin inflammation to study neutrophils and find a CXCR4hi population of NET-forming, phagocytic neutrophils whose induction depends on the transcription factor CREB1.

    • Jiaoling Chen
    • , Yaxing Bai
    •  & Shuai Shao

  • Article
    | Open Access

    Loss-of-function mutations in the chromatin remodelling protein HELLS result in humoral immune deficiency. Authors here show in a conditional knockout mouse model that HELLS controls the kinetics of a typical germinal center response by DNA methylation, its absence leading to either the appearance of memory-B cell markers or a metabolic state change typical of plasma cells.

    • Clara Cousu
    • , Eléonore Mulot
    •  & Sébastien Storck

  • Article
    | Open Access

    Allergic asthma is episodic and associated with seasonal changes which may have links with UV exposure levels. Here the authors propose a link between UVB exposure and ILC2 function through α-MSH released from the pituitary gland which accumulates in the serum and alters ILC2 function through the MC5R receptor.

    • Yuying Huang
    • , Lin Zhu
    •  & Bing Sun

  • Article
    | Open Access

    Galectin-3 (Gal-3) has been proposed to have a pathogenic role in systemic sclerosis (SSc). Here, the authors identify a Gal-3-based transcriptomic signature associated with SSc severity in patients and demonstrate that Gal-3 blockade reduces the severity of SSc skin and lung lesions in murine models.

    • Céline Ortega-Ferreira
    • , Perrine Soret
    •  & Frédéric De Ceuninck

  • Article
    | Open Access

    The most appreciated producers of pathogenic type-2 cytokines in asthma are T helper 2 cells and group 2 innate lymphoid cells, however, CD8+ cytotoxic T cells are also capable of secreting these mediators. Authors here show that IL-33, a cytokine that is produced by the inflammatory microenvironment, promotes type-2 cytotoxic T cell development, which is linked to asthma exacerbations.

    • Esmee K. van der Ploeg
    • , Lisette Krabbendam
    •  & Ralph Stadhouders

  • Article
    | Open Access

    The incidence of rheumatoid arthritis (RA) and accumulation of circulating free (cf) DNA increase with age but it is unknown whether DNA fragments cause joint inflammation. Here authors show that cf DNA levels are higher in RA patients and that in a rat adjuvant-induced arthritis model, the exonuclease TREX1 suppresses synovial inflammation via promoting the degradation of cf DNA and inhibiting a senescence-like cellular state.

    • Wei-Dan Luo
    • , Yu-Ping Wang
    •  & Vincent Kam Wai Wong

  • Article
    | Open Access

    Interleukin 9 (IL-9) is a cytokine that plays causative role in airway inflammation of both infectious and allergic origin. Here authors show in a mouse model of SARS-CoV-2 infection that IL-9, predominantly produced by helper T cells, plays a critical pathogenic role in COVID-19 via an inflammatory pathway involving the transcription factor Foxo1.

    • Srikanth Sadhu
    • , Rajdeep Dalal
    •  & Amit Awasthi

  • Article
    | Open Access

    Mutations that impact the function of the Arp2/3 complex are known to cause inborn errors of immunity. Here the authors describe biallelic null mutations in the ARPC5 subunit of Arp2/3 that disrupt actin function and cytokine signaling, causing infections, autoimmunity, inflammation and dysmorphisms.

    • Cristiane J. Nunes-Santos
    • , HyeSun Kuehn
    •  & Sergio D. Rosenzweig

  • Article
    | Open Access

    Inflammatory skin diseases are frequently associated with dysregulation of cutaneous immunity. Here the authors perform human challenge with house dust mite allergen in patients with atopic dermatitis and explore the molecular network determining tolerance versus inflammation and identify a role for metallothioneins in the modulation of allergen induced inflammation.

    • Sofia Sirvent
    • , Andres F. Vallejo
    •  & Marta E. Polak

  • Article
    | Open Access

    Mast cells are activated and proliferate during allergic reactions which can involve mast cell specific proteins. Here the authors show that mast cell-expressed membrane protein1 (MCEMP1) is an adaptor for KIT to promote SCF mediated mast cell proliferation and lack of MCEMP1 reduces inflammation in mouse asthma models.

    • Youn Jung Choi
    • , Ji-Seung Yoo
    •  & Jae U. Jung

  • Article
    | Open Access

    Neutrophilic inflammation is a hallmark of many monogenic autoinflammatory diseases. Here the authors report a case series of three unrelated boys with perinatal-onset of neutrophilic cutaneous small vessel vasculitis and systemic inflammation, and identify de novo truncating and missense variants in the Src-family tyrosine kinase LYN.

    • Adriana A. de Jesus
    • , Guibin Chen
    •  & Raphaela Goldbach-Mansky

  • Article
    | Open Access

    Antibodies directed against citrullinated proteins are commonly found in patients with rheumatoid arthritis. Here, the authors show that citrullination alters the peptide repertoire presented to T cells by altering protease cleavage and inducing protein destabilization, thereby exposing cryptic epitopes.

    • Ashley M. Curran
    • , Alexander A. Girgis
    •  & Erika Darrah

  • Article
    | Open Access

    The aetiology of primary biliary cholangitis (PBC) remains unclear. Here, the authors find that the numbers of DUOX2 + ACE2 + small cholangiocytes in human and mouse livers are inversely associated with disease severity, and present data indicating that they may be the target of polymeric immunoglobulin receptor (pIgR) -mediated humoral responses, suggesting that preservation of these cells and targeting anti-pIgR autoantibodies may be valuable strategies for therapeutic interventions in PBC.

    • Xi Li
    • , Yan Li
    •  & Jin Chai

  • Article
    | Open Access

    Inflammatory skin diseases involve various different immune cells in a localised area. Here the authors use spatial transcriptomics to show that disease relevant cytokine transcripts are sparsely expressed in lesional skin, yet are associated with local amplification cascades that promote skin inflammation.

    • A. Schäbitz
    • , C. Hillig
    •  & S. Eyerich

  • Article
    | Open Access

    Skin inflammation is often accompanied by systemic disease, yet the pathways that regulate this escalation are little known. Here authors show that transgenic expression of human CD1a in mice leads to the escalation of experimental skin inflammation and systemic inflammatory disease, and the generalized symptoms could be alleviated by blocking antibodies developed against CD1a.

    • Clare S. Hardman
    • , Yi-Ling Chen
    •  & Graham S. Ogg

  • Article
    | Open Access

    Low-dose interleukin-2 is showing promise in the treatment of several autoimmune inflammatory diseases. Here authors map the trajectory of cellular and transcriptional changes in type 1 diabetes patients receiving an interval dosing interleukin-2 regimen, which shows an anti-inflammatory gene expression signature shared by all immune cell types analysed, persisting for at least a month after ending treatment.

    • Jia-Yuan Zhang
    • , Fiona Hamey
    •  & Ricardo C. Ferreira

  • Article
    | Open Access

    Immune genes under selection can shed light on phenotypes contributing to survival and modern inflammatory conditions. Here, the authors prioritize adaptive disease variants in 535 risk loci for 21 inflammatory conditions and report promising SNPs for functional studies with predictions of cell context and function.

    • Vasili Pankratov
    • , Milyausha Yunusbaeva
    •  & Bayazit Yunusbayev

  • Article
    | Open Access

    Hyperferritinemic syndrome is a collective term for a group of severe inflammatory conditions distinguished by high ferritin levels, including adult-onset Still’s disease and COVID-19. Here authors show in an animal model that high ferritin levels are not just a sign of hyperinflammation but also a pathogenic factor that triggers neutrophil leukocyte activation and extracellular trap formation.

    • Jinchao Jia
    • , Mengyan Wang
    •  & Qiongyi Hu

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