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Volume 4 Issue 9, September 2003

All T cells require the calcineurin-NFAT pathway for normal activation. McKeon and colleagues (pages 874–881) show that calcipressin prevents NFAT (red) movement to the nucleus. Lack of calcipressin dysregulates Fas ligand expression, to which T helper type 1 (TH1) cells are particularly sensitive, leaving calcipressin-deficient mice with crippled TH1 responses. See also the News and Views by Parry and June (page 821). Artwork is acrylic on paper by Lewis Long.

Volume 4 Issue 9

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Editorial

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Correspondence

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News & Views

  • Early B cell development faces a critical checkpoint at the pro-B → pre-B transition stage, at which proper assembly and surface expression of an immunoglobulin heavy chain is somehow signaled by the pre-B cell receptor. Triggering of this signal might not require exogenous ligands.

    • Mark Schlissel
    News & Views

  • Growing evidence indicates immune and nervous systems use common mechanisms to mediate intercellular communication. Adding to this list is the discovery that dendritic cells modulate T cell interactions through expression of the neuronal receptor plexin-A1, which is regulated by the transcriptional activator CIITA.

    • Walter Reith
    News & Views

  • Calcineurin is negatively regulated by calcipressin 1. Analysis of calcipressin-deficient mice shows that survival of T helper type 1 cells is dependent on calcipressin, demonstrating another function for the regulation of calcineurin activity in T cells.

    • Richard V Parry
    • Carl H June
    News & Views

  • Members of the Toll-like receptor–interleukin 1 receptor superfamily signal inflammatory responses. However, a member of this family is now shown to modulate these responses by acting as a negative regulator.

    • Luke A J O'Neill
    News & Views

  • Interferon-α/β proteins are vital for innate immune responses to viruses. The tumor suppressor p53 mediates cell cycle arrest and apoptosis. A recent study in Nature reports that interferon-α/β stimulates p53 synthesis, demonstrating a hitherto unrecognized link.

    • Jan Vilček
    News & Views
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