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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.
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.
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.
The resolution of immune responses typically leaves a population of memory T cells to respond to subsequent infection. The generation of 'memory-like' T cells can also occur during homeostatic proliferation, but are they 'true' memory cells?
NKp46, an activating receptor expressed on natural killer cells, protects from lethal influenza virus infection. Contrary to prevailing views, involvement of NKp46 in tumor immunity is uncertain.