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Tumors and pathogens play a constant game of cat-and-mouse with their host's immune systems as they maneuver to gain the advantage. The strategies employed by both sides in this predator-prey equation are the centerpiece of this month's special Focus on Immune Evasion (pages 985–1049). This content and additional features are available free to registered users on the Nature Immunology website (www.nature.com/natureimmunology) through 1 February 2003.
This Focus issue brings together the cornucopia of strategies that pathogens and tumors utilize to avoid immune recognition. Here Rodney Phillips discusses some general principles that emerge from this analysis.
Signaling through antigen receptors was in the limelight from 4–8 May 2002 at the third EMBO workshop on “Lymphocyte antigen receptor and coreceptor signaling”. Key findings, new questions and emerging trends from the workshop are summarized here.
CTLA-4–Ig is used to block the costimulation of T cells to interfere with their activation. This reagent may actually be working by provoking DCs to catabolize tryptophan, thereby depriving T cells and contributing to their demise.
Lipid second messengers are thought to be important in T cell activation. Two studies show the spatial-temporal organization of these lipids during immunological synapse formation and raise new questions about their functions.
A series of comprehensive reviews examining mechanisms of immune escape. The juxtaposition of tumor with microbial immune evasion reveals the many parallels between the different systems.