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Volume 7 Issue 2, February 2006

Genetic approaches for identifying immune functions can yield unexpected findings. Beutler and colleagues (p. 156; News and Views by Tough, p 127) characterize '3d', a mutation that alters the endoplasmic reticulum protein UNC-93B (yellowish green). This protein is not found in lysosomes or acidified endosomes (red) and is required for both Toll-like receptor signaling and exogenous antigen presentation. Original image by Benjamin E. Steinberg. Artwork by Lewis Long.

Volume 7 Issue 2

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Editorial

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Meeting Report

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News & Views

  • Substitutions in CD8+ T cell epitopes in viral proteins can alter the complex interaction between viruses and host immunity. Reduced viral fitness and recognition of altered and subdominant epitopes are possible outcomes.

    • Joel N Blankson
    • Justin R Bailey
    • Robert F Siliciano
    News & Views

  • Suppressor of cytokine signaling 1 has been linked to the negative regulation of Toll-like receptor signaling. The mechanism for this seems to be suppressor of cytokine signaling 1–mediated degradation of the adaptor Mal, which is required for Toll-like receptor signaling.

    • Takashi Kobayashi
    • Giichi Takaesu
    • Akihiko Yoshimura
    News & Views

  • Naive CD8+ T cells can be activated via dendritic cell 'cross-priming' of antigens obtained exogenously. Dendritic cells cannot cross-prime, however, after systemic activation in vivo, potentially contributing to immunosuppression associated with severe infections.

    • Heather D Hickman-Miller
    • Jonathan W Yewdell
    News & Views

  • 'Forward' genetic approaches for elucidating function can lead to unexpected findings. A single missense mutation is found to disrupt both antigen presentation and nucleic acid Toll-like receptor signaling, two processes involving endocytic pathways.

    • Robert W Carter
    • David F Tough
    News & Views
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