Volume 5 Issue 9, September 2004

Volume 5 Issue 9

Nuclei stained for the presence of PIAS1 (green), a protein that binds to STAT1. Interferons protect the host through STAT-mediated induction of many other genes. Shuai and colleagues (p 891; News and Views by O'Shea p 875) identified a subset of genes stifled by PIAS1. The discriminating PIAS1 had a surprisingly large in vivo effect, making it a potential therapeutic target. Artwork by Lewis Long, inspired by immunofluorescence micrograph from Shuai and colleagues.




  • Commentary |

    The natural history of human immunodeficiency virus (HIV) infection has been altered through the development of drugs targeting two key viral enzymes, reverse transcriptase and protease. Continued advances from basic science have unearthed many other points of attack in the HIV life cycle that could lead to new classes of HIV therapeutics.

    • Warner C Greene

News and Views

  • News & Views |

    CD4+ T cells reportedly program CD8+ T cells to develop into suitable memory cells during the primary immune response. However, new data indicate that the maintenance of CD8+ memory T cells requires continuous exposure to bystander CD4+ T cells.

    • Sara E Hamilton
    • , Martin Prlic
    •  & Stephen C Jameson
  • News & Views |

    Members of the PIAS family can negatively regulate the cytokine-activated Jak-STAT pathway in vitro. One member of this family, PIAS1, is a nonredundant and physiologic regulator of certain STAT1-dependent interferon-induced genes.

    • John J O'Shea
    •  & Wendy Watford
  • News & Views |

    A recent paper in Nature identifies replication protein A as the key binding partner of AID for B cell somatic hypermutation.

    • Jean-Claude Weill
    •  & Claude-Agnès Reynaud
  • News & Views |

    Although CD4+ T cell help is required for effective pathogen control, persistent antiviral CD4+ T cell help can, paradoxically, impair the generation of neutralizing antibody responses and thus potentially limit protective immunity.

    • Dirk Homann
    •  & Ronald G Gill