Autoimmunity articles within Nature Communications

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  • Article
    | Open Access

    Natural killer (NK) cells eliminate damaged cells, but spare healthy ones by recognizing their expressed ligands via NK inhibitory receptors. Here the authors solve the structure of an NK inhibitory receptor, NKR-P1B, bound to its ligand, Clr-b, with further data suggesting a weak interaction and informing on the basis of missing-self recognition.

    • Gautham R. Balaji
    • , Oscar A. Aguilar
    •  & Richard Berry

  • Article
    | Open Access

    T cell functions depend on distinct metabolic fluxes. Here the authors show different metabolic requirements of humoral responses to self versus microbial antigens: while glucose is dispensable for antiviral Tfh and antibody responses, it is essential to mount these responses against autoantigens.

    • Seung-Chul Choi
    • , Anton A. Titov
    •  & Laurence Morel

  • Article
    | Open Access

    Conventional B cells express clonally specific antigen receptors, but a small subset of B cells from patients and mice with systematic lupus erythematosus simultaneously expresses two distinct antigen receptors. Here the authors show that these dual-specificity B cells have higher levels of MHC-II, depend on IL-21 for expansion, and mount stronger memory response.

    • Allison Sang
    • , Thomas Danhorn
    •  & Roberta Pelanda

  • Article
    | Open Access

    Roquin targets are known to contain two types of sequence-structure motifs, the constitutive and the alternative decay elements (CDE and ADE). Here, the authors describe a linear Roquin binding element (LBE) also involved in target recognition, and show that Roquin binding affects the translation of a subset of targeted mRNAs.

    • Katharina Essig
    • , Nina Kronbeck
    •  & Vigo Heissmeyer

  • Article
    | Open Access

    Regulatory T cells are crucial for the establishment and maintenance of peripheral immune tolerance, yet the mechanisms regulating their stability and function remain to be fully elucidated. Here the authors show SENP3 maintains Treg cell stability and function via BACH2 deSUMOylation.

    • Xiaoyan Yu
    • , Yimin Lao
    •  & Qiang Zou

  • 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

    Germinal center (GC) is where B cells interact with other immune cells for optimal induction of antibody responses. Here the authors show that galectin-3 regulates GC development by modulating interferon-γ and B cell-intrinsic signaling, such that galectin-3 deficiency mice exhibit lupus-like autoimmune symptoms.

    • Cristian Gabriel Beccaria
    • , María Carolina Amezcua Vesely
    •  & Adriana Gruppi

  • Article
    | Open Access

    T help 17 (Th17) cells are important mediators for both protective and pathogenic immune reactions, but how their functions are regulated at the epigenetic level is not understood. Here the authors show that TRIM28, a cofactor for transcriptional regulation, is important for epigenetic activation of Th17-related gene loci during Th17 response.

    • Yu Jiang
    • , Ying Liu
    •  & Chen Dong

  • Article
    | Open Access

    Blocking B-cell activating factor (BAFF), an important soluble factor for B-cell responses, with specific antibodies is approved for treating autoimmune disorders. Here the authors show, with structural data, that antibody-BAFF interactions not only interrupt BAFF–receptor-binding, but also induce the formation of a less active BAFF polymer.

    • Woori Shin
    • , Hyun Tae Lee
    •  & Yong-Seok Heo

  • Article
    | Open Access

    Systemic lupus erythematosus (SLE) is an autoimmune disorder mediated by excessive autoantibodies. Here the authors show that an E3 ubiquitin ligase, Peli1, negatively modulates noncanonical NF-κB signaling to restrain lupus-like symptoms in mice, and that Peli1 expression inversely correlates with SLE severity in humans.

    • Junli Liu
    • , Xinfang Huang
    •  & Yichuan Xiao

  • Article
    | Open Access

    Regulatory B cells (Breg) are known to suppress immune responses by secreting interleukin-10 (IL-10). Here the authors show that, alternatively, Bregs may also present lipid antigens on surface CD1d to induce IFN-γ production from invariant natural killer cells to ameliorate experimental arthritis via IL-10-independent pathways.

    • K. Oleinika
    • , E. C. Rosser
    •  & C. Mauri

  • 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

    Inflammasomes are protein complexes induced by pathogens for the secretion of pro-inflammatory cytokines IL-1β and IL-18 in immune cells. Here the authors show, using a new mouse model, that aberrant NLRC4 and ASC-dependent inflammasome activation in neutrophils contributes to systemic inflammation.

    • Randilea D. Nichols
    • , Jakob von Moltke
    •  & Russell E. Vance

  • Article
    | Open Access

    Circadian controls of immune responses by the molecular clock have been reported, but the underlying mechanisms are unclear. Here the authors show that the master circadian gene, Bmal1, is essential for modulating the homeostasis of myeloid cells to control pro-inflammatory IL-17+/IFN-γ+ T cells in autoimmunity.

    • Caroline E. Sutton
    • , Conor M. Finlay
    •  & Annie M. Curtis

  • Article
    | Open Access

    T cell receptors are generated by somatic gene recombination, and are normally selected against autoreactivity. Here the authors show that CD4 T cells from patients with autoimmune type 1 diabetes have shorter TCRβ sequences, broader repertoire diversity, and more repertoire sharing than those from healthy individuals.

    • Iria Gomez-Tourino
    • , Yogesh Kamra
    •  & Mark Peakman

  • Article
    | Open Access

    Autoimmune anaemia often accompanies Plasmodium infection and malaria, but how anaemia is induced is still unclear. Here the authors show that Plasmodium DNA, together with interferon-γ, can activate B cells to induce auto-antibodies that recognize red blood cells and promote their removal to contribute to anaemia onset.

    • J. Rivera-Correa
    • , J. J. Guthmiller
    •  & A. Rodriguez

  • Article
    | Open Access

    Follicular helper T (TFH) cells promote germinal centre (GC) response for efficient generation of protective antibodies during humoral immunity. Here the authors show that deficiency of the translational repressor, Capicua/CIC, enhances TFH differentiation and GC responses potentially via the derepression of Etv5.

    • Sungjun Park
    • , Seungwon Lee
    •  & Yoontae Lee

  • Article
    | Open Access

    The protein kinase Lkb1 has been shown to limit conventional T cell activation and pro-inflammatory functions. Here the authors show that Lkb1 also maintains Foxp3 expression and suppressive function in regulatory T (Treg) cells, and that Treg-specific Lkb1-deficient mice develop fatal autoimmune disease.

    • Di Wu
    • , Yuechen Luo
    •  & Xiaoming Feng

  • Article
    | Open Access

    The transcriptional program activated by Smad2/Smad3 is critical for the induction and function of regulatory T cells. Here the authors show that the expression of Smad3 is modulated by the complementary functions of a methyltransferase Ash1l and an lncRNA lnc-Smad3 on the promoter accessibility of the mouseSmad3locus.

    • Meng Xia
    • , Juan Liu
    •  & Xuetao Cao

  • Article
    | Open Access

    IL-17-producing γδ T (γδT17) cells position in barrier tissues but also home to inflammatory sites. How this trafficking is regulated is unclear. Here the authors show that the dynamic expression of chemokine receptors CCR2 and CCR6 differentiates γδT17 cell trafficking patterns at homeostasis and in inflammatory scenarios.

    • Duncan R. McKenzie
    • , Ervin E. Kara
    •  & Shaun R. McColl

  • Article
    | Open Access

    T regulatory (Treg) cells are essential for maintaining immune homeostasis, but how the stability of their lineage and function is regulated is unclear. Here the authors show that Ndfip1 is essential for suppressing Tregcell IL-4 production and metabolic alteration to preserve Treg lineage and function.

    • Awo Akosua Kesewa Layman
    • , Guoping Deng
    •  & Paula M. Oliver

  • Article
    | Open Access

    T helper 17 (Th17) cells can be pathogenic, but what controls this phenotype is unclear. Here the authors show that the transcription factor JunB promotes proinflammatory Th17 function by regulating the transcription of multiple Th17-related genes.

    • Zafrul Hasan
    • , Shin-ichi Koizumi
    •  & Hiroki Ishikawa

  • Article
    | Open Access

    Antibodies against the platelet factor 4 (PF4) support bacterial host defence but in some cases may lead to heparin-induced thrombocytopenia (HIT). Nguyenet al.show that in autoimmune HIT a subset of antibodies binds strongly to PF4 causing its conformational change that leads to association of non-pathogenic PF4 antibodies and thrombotic platelet activation.

    • Thi-Huong Nguyen
    • , Nikolay Medvedev
    •  & Andreas Greinacher

  • Article
    | Open Access

    Neurons can convert pathogenic T cells to anti-inflammatory FoxA1+ regulatory T cells (Tregs), which can ameliorate EAE, but the molecular mechanism is only partially understood. Liu et al. show that autocrine interferon β signalling induces PDL1 expression in neurons, which is essential for neurons to reprogramme pathogenic T cells to FoxA1+ Tregs.

    • Yawei Liu
    • , Andrea Marin
    •  & Shohreh Issazadeh-Navikas

  • Article
    | Open Access

    Ca2+ release-activated Ca2+(CRAC) channels are essential for protective immunity, but the immunological functions of the three ORAI homologues that form CRAC channels are unclear. Here the authors show that ORAI1 and ORAI2 form heteromeric CRAC channels, which fine-tune T cell activation and immune responses.

    • Martin Vaeth
    • , Jun Yang
    •  & Stefan Feske

  • Article
    | Open Access

    The immunosuppressive role of regulatory T (Treg) cells largely depends on their virtue of expressing the transcription factor FOXP3. Here the authors show that the E3 deubiquitinase USP21 stabilizes FOXP3 by mediating its deubiquitination and helps to maintain the expression of Treg signature genes and Treg lineage stability in mice.

    • Yangyang Li
    • , Yue Lu
    •  & Bin Li

  • Article
    | Open Access

    Naïve T cells establish self-tolerance via negative selection of cells with strong reactivity for self-peptide/MHC complexes, but undergo T-cell receptor (TCR) desensitisation when leaving the thymus. Here, Choet al.show that TCR desensitisation correlates with cell-surface density of the phosphatase CD45.

    • Jae-Ho Cho
    • , Hee-Ok Kim
    •  & Jonathan Sprent

  • 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

    ICER is a CREM splice variant that represses CREM/CREB signalling. Here the authors use human cells and mouse models of various autoimmune diseases to show that ICER is central to pathogenic Th17 cell differentiation in autoimmunity.

    • Nobuya Yoshida
    • , Denis Comte
    •  & George C. Tsokos

  • Article
    | Open Access

    Roquin is an RNA-binding protein that prevents autoimmunity by limiting expression of receptors such as Ox40. Here, the authors identify an RNA structure that they describe as an alternative decay element, and they characterise its interaction with Roquin using structural and biochemical techniques.

    • Robert Janowski
    • , Gitta A. Heinz
    •  & Michael Sattler

  • Article
    | Open Access

    Autoimmune brain inflammation is associated with activation of macrophages and microglia. Here the authors show that fibrinogen induces encephalitogenic T-cell activation and macrophage recruitment to the central nervous system, and promotes demyelination in a mouse model of multiple sclerosis.

    • Jae Kyu Ryu
    • , Mark A. Petersen
    •  & Katerina Akassoglou

  • Article
    | Open Access

    T cells that are activated by self-antigens in the periphery can migrate into the brain causing neuroinflammatory disease. Here the authors show that TBK1 is necessary for activated T-cell egress from the lymph node, and blocking TBK1 ameliorates autoimmunity in a mouse model of multiple sclerosis.

    • Jiayi Yu
    • , Xiaofei Zhou
    •  & Shao-Cong Sun

  • Article |

    Whether differentiation of regulatory and conventional T cells in the thymus requires similar T-cell receptor affinity is not known. Here, the authors show that cells expressing the same T-cell receptor selected on the same ligand can give rise to both lineages, but different sensitivity to negative selection separates their T-cell receptor repertoires.

    • Lukasz Wojciech
    • , Alicja Ignatowicz
    •  & Leszek Ignatowicz

  • Article
    | Open Access

    Regulatory T cells (Tregs) are important for the maintenance of self-tolerance and this requires their trafficking to the lymph nodes and target tissues. Here, the authors show that the recognition of self-antigens expressed by endothelial cells in target tissue is instrumental for efficient Treg recruitment in vivo.

    • Hongmei Fu
    • , Madhav Kishore
    •  & Federica M. Marelli-Berg

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