Autoimmune diseases articles within Nature Communications

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  • Article
    | Open Access

    B-cell maturation antigen (BCMA) regulates the survival of B cells and is essential for the maintenance of long-lived plasma cells. Here, the authors show that γ-secretase directly sheds BCMA from the cell surface and therefore regulates the number of plasma cells.

    • Sarah A. Laurent
    • , Franziska S. Hoffmann
    •  & Edgar Meinl

  • Article |

    Multiple sclerosis is caused by autoreactive Th17 lymphocytes. Here the authors show that prostaglandin E2 promotes Th17 differentiation by activating transcription of IL-17 by CREB/CRTC2 complex, and that ablation of CRTC2 prevents Th17 differentiation and multiple sclerosis in a mouse model.

    • Jeniffer B. Hernandez
    • , Christina Chang
    •  & Marc Montminy

  • Article
    | Open Access

    Dendritic cells are critical for initiation of immune responses and for induction of tolerance. Here the authors show that deletion of survival factor c-flip in CD11c-expressing cells subset perturbs CD8a+dendritic cell, NK and macrophage pools, and leads to development of autoimmune arthritis.

    • Qi-Quan Huang
    • , Harris Perlman
    •  & Richard M. Pope

  • Article |

    Compromised function of regulatory T cells can lead to autoimmunity. Here the authors show that miR-125a stabilizes regulatory T-cell function and is downregulated in lupus and Crohn’s disease, as well as autoimmune mouse models, and that a chemical miR-125a analogue reverts established disease in a mouse model of multiple sclerosis.

    • Wen Pan
    • , Shu Zhu
    •  & Nan Shen

  • Article |

    Self-reactive B cells producing autoantibodies are associated with autoimmune conditions. Here, the authors show that in mice lacking the surrogate light chain, which normally assembles with antibody heavy chain to form a pre-B-cell receptor, the autoantibody-producing cells derive from germinal centres.

    • Ola Grimsholm
    • , Weicheng Ren
    •  & Inga-Lill Mårtensson

  • Article |

    Autoantibodies targeting citrunillated proteins are common in rheumatoid arthritis patients. Here the authors show that vinculin (a human protein) and some microbial proteins are recognized by these antibodies and by CD4+T cells, and this response is absent in patients carrying a protective HLA allele.

    • Jurgen van Heemst
    • , Diahann T. S. L. Jansen
    •  & René E. Toes

  • Article
    | Open Access

    FcγRs are cell-surface receptors for IgGs that play key roles in the humoral and cellular immune response to infection. Here, the authors present a high-resolution crystal structure of the hFcγRI-Fc complex to reveal the molecular mechanisms underlying the high specificity of this important immunological interaction.

    • Masato Kiyoshi
    • , Jose M.M. Caaveiro
    •  & Kouhei Tsumoto

  • Article |

    Histone deaceytelase inhibitors are used in the treatment of haematological malignancies but can also act as modulators of the immune system. Here, the authors show that histone deaceytelase inhibitors are capable of modulating B-cell functions leading to improved outcome in autoimmune conditions.

    • Michaela Waibel
    • , Ailsa J. Christiansen
    •  & Edwin D. Hawkins

  • Article
    | Open Access

    The IgG sugar moiety modulates the binding of immune complexes to their Fcγ receptors resulting in pro- or anti-inflammatory response. This study shows that IgG sialylation also affects osteoclastogenesis and bone mass in mice and humans, identifying a new link between bone and the immune system.

    • Ulrike Harre
    • , Stefanie C. Lang
    •  & Georg Schett

  • Article
    | Open Access

    B cells reactive against self antigens can cause autoimmune disease, but are normally suppressed by regulatory T cells (Tregs). Here the authors show that a subset of Tregs can suppress lupus in a mouse model by making TGF-β3 cytokine and by engaging an inhibitory PD-1 receptor on B cells.

    • Tomohisa Okamura
    • , Shuji Sumitomo
    •  & Kazuhiko Yamamoto

  • Article |

    TLR7 triggers immune responses upon sensing microbial RNA, and its endosomal localization is thought to prevent TLR7 activation by host RNA. Here, Kanno et al. show that TLR7 is also present on the surface of immune cells, and that anti-TLR7 antibody can prevent TLR7-mediated autoimmunity.

    • Atsuo Kanno
    • , Natsuko Tanimura
    •  & Kensuke Miyake

  • Article |

    Follicular helper T cells promote antibody production by B cells, and regulatory B cells, in turn, can restrain T cell activation. Here, Khan et al. show that PD-L1 plays a critical role in regulatory B cell function, curbing excessive immune responses by engaging the PD-1 receptor on follicular helper T cells.

    • Adnan R. Khan
    • , Emily Hams
    •  & Padraic G. Fallon

  • Article |

    LL37 is an antimicrobial peptide that is overexpressed in skin lesions from psoriasis patients and activates innate immunity. Here the authors show that CD4 and CD8 T cells specific for LL37 are present in the circulation of patients with psoriasis, produce inflammatory cytokines and correlate with disease activity.

    • Roberto Lande
    • , Elisabetta Botti
    •  & Loredana Frasca

  • Article
    | Open Access

    Protein scaffolds can serve as alternatives to antibodies in a range of applications. Here, the authors report the design and development of Alphabody™, a protein scaffold featuring a single-chain antiparallel triple-helix coiled-coil fold that the authors use to develop Alphabodies that can neutralize human IL-23 with high specificity and affinity.

    • Johan Desmet
    • , Kenneth Verstraete
    •  & Savvas N. Savvides

  • Article
    | Open Access

    The mechanism by which NAD+ alters the systemic immune response is unclear. Here the authors show that NAD+ induces systemic homeostasis and protects against experimental autoimmune encephalomyelitis, a mouse model of multiple sclerosis, by regulating CD4+T cell differentiation and promoting myelin and axonal regeneration.

    • Stefan G. Tullius
    • , Hector Rodriguez Cetina Biefer
    •  & Abdallah ElKhal

  • Article |

    Genetic studies have connected polymorphisms in the IL-2 receptor alpha (IL2RA) gene with susceptibility to multiple sclerosis, but the mechanisms underlying this association are not clear. Here, the authors show that a polymorphism in IL2RA increases responsiveness to IL-2 and GM-CSF production in human THcells.

    • Felix J. Hartmann
    • , Mohsen Khademi
    •  & Burkhard Becher

  • Article
    | Open Access

    Coeliac disease is characterized by an inappropriate immune response to dietary gluten proteins, involving the production of antibodies reactive to gluten. Here, the authors study the intestinal antibody response against gluten and show that gluten-specific antibodies have a low degree of somatic hypermutations.

    • Øyvind Steinsbø
    • , Carole J. Henry Dunand
    •  & Ludvig M. Sollid

  • Article
    | Open Access

    Mouse models of arthritis generally do not result in both chronic disease and autoantibody production—two key features of the human disease. Here the authors obtain both features by combining two common protocols, and find that disease severity is associated with the presence of a previously unidentified lymph node.

    • Uta Baddack
    • , Sven Hartmann
    •  & Gerd Müller

  • Article
    | Open Access

    Complex diseases such as multiple sclerosis have both genetic and environmental components. This study demonstrates that variants of genes implicated in multiple sclerosis, and alterations in cellular metabolism and vitamin D3 levels, alterN-glycosylation, a post-translational modification causal of the disease in mice.

    • Haik Mkhikian
    • , Ani Grigorian
    •  & Michael Demetriou

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