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Volume 9 Issue 2, February 2008

Although tightly regulated in healthy animals, leukocyte migration into the central nervous system runs awry in neuroinflammatory disorders. Prat and colleagues (p 137) show that ALCAM, an adhesion molecule expressed on blood-brain barrier endothelial cells, promotes the entry of pathogenic leukocytes into the central nervous system. The original micrograph shows human CD4+ T cells (green) migrating across human blood-brain barrier endothelial cells expressing ALCAM (red) in vitro. Artwork by Lewis Long.

Volume 9 Issue 2

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  • Authors should provide a cover letter that explains 'in their words' why the new work should be published in a top-tier journal.

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  • Lymphocytes depend on endothelial adhesion molecules such as ICAM-1 and VCAM-1, upregulated with inflammation, to facilitate transmigration across junctional barriers. New data show that ALCAM replaces VCAM-1 in the CNS during the development of neuroinflammatory diseases such as multiple sclerosis.

    • Boris P-L Lee
    • Beat A Imhof
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  • The prevailing paradigms ascribe the initiation of immune surveillance to the detection of foreign or inflammatory 'danger' signals. However, new work indicates that immune cells can detect early signs of cellular dysregulation that precede tumorigenesis, even in the absence of non-self signals and/or inflammation.

    • Daniel M Andrews
    • Mark J Smyth
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  • Inducible regulatory T cells respond to TGF-β by upregulating Foxp3 expression. Tone and colleagues identify an enhancer site in Foxp3 that binds transcription factors Smad3 and NFAT, suggesting a means by which TGF-β regulates Foxp3 expression.

    • Harald von Boehmer
    • Jens Nolting
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  • The T cell costimulatory protein LIGHT and coinhbitory protein BTLA share a common ligand, HVEM. Now CD160 is also shown to bind HVEM and deliver a potent inhibitory signal to CD4 T cells.

    • Jonathan Kaye
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  • The inflammatory cytokine interleukin 17, normally considered a T cell–associated factor, is now reported to be the central participant driving the development of germinal center–derived autoantibodies in a model disease setting.

    • David Tarlinton
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