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Whether RNA interference is an important component of the drosophila defense against virus infection in vivo has been unclear. Imler and colleagues (p 590) now demonstrate that for certain virus infections,RNA interference is a critical defense mechanism in flies. Fat body cells (nuclei in red) are shown infected with Sindbis virus (E1 glycoprotien in green). Art work by Lewis Long, inspired by an immunofluoresence micrograph by Imler and colleagues.
Robert L. Coffman recounts how his work on immunoglobulin E regulation along with data from Tim Mosmann on the functional heterogeneity of T cell clones led to the T helper type 1–T helper type 2 hypothesis.
Disease-oriented, introductory medical curricula can help overcome educational and institutional barriers that separate aspiring translational scientists in PhD programs from the world of medicine.
Immune responses to bacterial infection occur by host cell detection of bacterial components. Monomeric flagellin can be elicited directly by host cells and then are 'sensed' by the cytosolic protein Ipaf.
Dendritic cells initiate immune responses but also influence regulatory T cell activity and homeostasis. Functional outcomes of dendritic cell–T cell interactions depend on the immunological context of their encounter.
The integrated stress response is a complex signaling pathway that regulates myriad cell processes, including protein translation, depending on the stress conditions. Primed CD4+ T helper cells may use this response system to optimize cytokine expression.
To prevent RNA virus–dependent tissue damage caused by interferon-regulatory factor 3 (IRF3)–induced type I interferons, proteasome-dependent destruction of IRF3 is orchestrated by the cytoplasmic prolyl isomerase Pin1.
T helper cells that produce interleukin 17 can promote a range of immune-mediated inflammatory diseases. Papers in Nature and Immunity suggest transforming growth factor-β promotes the differentiation of these pathogenic cells.