Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Caenorhabditis elegans (pictured) has an innate system for immune defense. Ewbank and colleagues (p 488; News and Views by Hodgkin p 471) use this powerful genetic model to show that the worm ortholog of SARM, a vertebrate TIR adaptor protein of unknown function, controls the induction of antimicrobial peptides in a Toll-like receptor-independent way. Artwork by Lewis Long.
Vaccination is a marvel of scientific endeavor that benefits the masses. Yet the laissez-faire economy may not provide a sufficient push for vaccine research and development. The current climate that drives this globally important venture is examined here.
An ideal vaccine has certain biological and physical characteristics. Technological advances have provided new strategies that may help the design of such a vaccine.
Vaccination has attracted controversy at every stage of its development and use. Ethical debates should consider its basic goal, which is to benefit the community at large rather than the individual.
The idea that Qa-1-dependent CD8+ suppressor T cells regulate peripheral immune responses was unpopular during the era of 'suppressor skepticism' in the late 1980s, but this has now been resurrected.
The function of the mammalian TIR domain adaptor protein SARM is unclear. In Caenorhabditis elegans, however, the homolog of SARM controls the induction of peptides involved in innate immunity.
Toll-like receptors (TLRs) use multiple downstream signaling pathways. New data suggest that components of the tumor necrosis factor receptor signaling pathway are involved in signal transduction by certain TLR family members.
Correlative analyses of polymorphism and disease resistance in Drosophila melanogaster refine our understanding of the forces that maintain variation in innate immunity loci.
Antigen receptor genes are assembled by a sequence of lineage-specific recombinatorial events, in which DNA breaks must be properly repaired to ensure cell survival and further developmental maturation. B lymphocytes, it seems, use multiple unique pathways to repair their DNA.