Autoimmunity articles within Nature

Featured

  • Letter |

    The transcription factor Foxo1 is shown to be involved in the determination of distinct subsets of regulatory T (Treg) cells, and the differentiation of activated phenotype Treg cells is associated with the repression of the Foxo1-dependent transcriptional program; constitutively active Foxo1 expression triggers depletion of activated Treg cells in peripheral tissues and leads to CD8 T-cell-mediated autoimmunity and anti-tumour immunity.

    • Chong T. Luo
    • , Will Liao
    •  & Ming O. Li
  • Article |

    Autoantigen-presenting dendritic cells are shown to interact with both effector and regulatory T cells, and effector-produced IL-2 activates the transcription factor STAT5 in regulatory T cells, which in turn upregulates suppressive molecules and prevents autoimmunity.

    • Zhiduo Liu
    • , Michael Y. Gerner
    •  & Ronald N. Germain
  • Letter |

    Diverse autoimmune and allergic diseases are associated with polymorphisms in a locus encoding the transcription factor BACH2; here, BACH2 is shown to be a broad regulator of immune activation that stabilizes the differentiation of Treg cells by repressing commitment of CD4+ T cells to alternate cell fates.

    • Rahul Roychoudhuri
    • , Kiyoshi Hirahara
    •  & Nicholas P. Restifo
  • Letter |

    A search for variants in coding exons of 25 genome-wide association study risk genes in a large cohort of autoimmune patients finds that rare coding-region variants at known loci have a negligible role in common autoimmune disease susceptibility, arguing against the previously proposed rare-variant synthetic genome-wide association hypothesis.

    • Karen A. Hunt
    • , Vanisha Mistry
    •  & David A. van Heel
  • Letter |

    Transcriptional profiling of developing TH17 cells identifies serum glucocorticoid kinase 1 (SGK1) as an essential node downstream of IL-23 signalling, and transcriptional analysis shows that a modest increase in salt concentration induces SGK1 expression, promotes IL-23 receptor expression and enhances TH17 cell differentiation, accelerating the development of autoimmunity.

    • Chuan Wu
    • , Nir Yosef
    •  & Vijay K. Kuchroo
  • Letter |

    Increased salt concentrations are shown to induce murine and human TH17 cells by a mechanism that depends on activation of p38/MAPK, NFAT5 and SGK1; mice kept on a high-salt diet develop a more severe experimental autoimmune encephalomyelitis due to increased induction of TH17 cells.

    • Markus Kleinewietfeld
    • , Arndt Manzel
    •  & David A. Hafler
  • Comment |

    Joel V. Weinstock explains why several clinical trials are deliberately infecting people with helminths to treat autoimmune diseases.

    • Joel V. Weinstock
  • Outlook |

    Scientists have some way to go before they can prove that COPD should be treated as an autoimmune disease, says Steven R. Duncan.

    • Steven R. Duncan
  • Outlook |

    Many COPD patients are deficient in vitamin D, a condition that can lead to bone problems as well as difficulty breathing. Can dietary supplements be of help?

    • Thea Singer
  • News & Views |

    In multiple sclerosis, the body's own immune cells attack the brain and spinal cord. But how they get there from peripheral tissues has been a mystery. Surprisingly, the lungs might be a key transit point. See Letter p.675

    • Richard M. Ransohoff
  • Letter |

    Mature B cells encounter antigens during development that induce anergy or functional unresponsiveness; this large reservoir of dormant autoreactive B cells may serve as a pool of extended antibody specificity for purposes of protective immunity, as well as the source of pathogenic autoantibodies that characterize rheumatic diseases such as systemic lupus erythematosus.

    • Julie Zikherman
    • , Ramya Parameswaran
    •  & Arthur Weiss
  • Letter |

    Thymus-derived regulatory T cells are activated by recognition of peripheral self antigen, persist in the target tissue on cessation of antigen exposure, and respond to re-exposure to self antigen with enhanced functional activity.

    • Michael D. Rosenblum
    • , Iris K. Gratz
    •  & Abul K. Abbas
  • Letter |

    Sialic acid acetylesterase (SIAE) is an enzyme that is involved in B-cell activation and is required to maintain immunological tolerance in mice. It is shown here that rare, inherited and functionally defective SIAE variants are associated with a variety of autoimmune diseases in humans. The study provides one of the first examples of the importance of rare genetic variants in complex diseases, such as those involving autoimmunity.

    • Ira Surolia
    • , Stephan P. Pirnie
    •  & Shiv Pillai