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Some viral infections destroy lymph node stromal cells. Scandella et al. (p 667) demonstrate that the restoration of lymph node integrity requires lymphoid tissue-inducer cells and signaling via lymphotoxin α1β2. Original image shows splenic sections immunostained for B220 (blue) and Thy-1.2 (green) to define B and T cell zones and with anti-gp38 to visualize T cell zone stromal cells. Original image by Elke Scandella. Artwork by Lewis Long.
Harald von Boehmer describes how he used mice transgenic for T cell receptor αβ to identify T cell receptor–dependent cellular selection and lineage commitment as mechanisms responsible for generating an effective and self-tolerant adaptive immune system.
The need to translate basic research in the field of human immunology may be much more urgent, and the rewards potentially much greater, than is often acknowledged. Yet a commonly perceived coercion to undertake translational research may be unhelpful. Instead, we propose clear incentives for integrating key skill sets, together with achievable cultural adjustments in research and medicine that span training, recruitment and promotion.
Toll-like receptors trigger an innate immune response by activating signaling pathways that are dependent on IRAK kinases. According to Kawagoe et al., the least understood IRAK member, IRAK2, is required for the perpetuation of these signals.
The T cell receptor (TCR) is functionally coupled to a constellation of ten immunoreceptor tyrosine–based activation motifs (ITAMs). A new study suggests that this large number of ITAMs is mandatory for preventing autoimmunity.
B cell tolerance is achieved in part through secondary rearrangements that replace ('edit') exons encoding autoreactive antigen-receptor chains. New findings suggest that Foxo transcription factors are critical regulators of receptor editing by activating the transcription of recombination-activating genes.
Three new studies demonstrate that development of human TH-17 cells requires transforming growth factor-β and one or more proinflammatory cytokines, which are the same requirements as for mouse TH-17 development.