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.
How do T cells that are specific for pancreatic islet cell antigens cause diabetes? A recent paper in Nature provides evidence from NOD mice that the killer T cells responsible increase their avidity as the disease progresses—removing the high avidity clones prevents disease.
The question of how we acquire immunity has been investigated for a century or more. What have we learned from all of this endeavor? We asked Rolf Zinkernagel to provide, for the young investigator, food for thought about that which we still don't know—even if we think we do.
Perturbation of T cell differentiation by overexpression of SCL and LMO can lead to leukemia. This dysregulation may be initiated by inactivation of E2A.
Much vaccine research is directed toward the generation of more effective vaccines. By combining DNA vaccines with the innate immune system, a flu vaccine was designed that required only a single immunization.
Historical Insight: The immunologic relationship between the fetus and its parents has fascinated investigators for generations. Early experiments by Ehrlich, as recounted here by Arthur Silverstein, clarified some crucial issues and paved the way for studies that are still ongoing today.
Tumor vaccines comprised of the chaperone gp96 can instigate specific immunity to tumor peptides. A receptor on macrophages for the uptake of peptide-loaded gp96 has been identified as CD91, the α2-macroglobulin receptor.
NK cells become cytotoxic upon receiving a signal through their activation receptors. The orphan proteins H-60 and Rae1 have now been identified as ligands for the mouse NKG2D activation receptor. Remarkably they are inducible and may be blocked by a viral protein.