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Escherichia coli is the cause of most urinary-tract infections (UTIs). Consequent renal disease is a major cause of renal failure, due partly to the inflammatory response to infection. On page 801 of this issue, Springall et al. investigate the role of complement in ascending UTIs. Complement-deficient mice show limited E. coli infection in the upper urinary tract and endogenous C3 enhances the bacterium-epithelial-cell interaction. The cover photo is a scanning electron micrograph of E. coli (x28,600).
A mouse model for donor lymphocyte infusion reveals that a single immunodominant minor H antigen is responsible for the beneficial effects of donor T lymphocytes against host leukemia. Separating the good from the bad could mean the end of graft-versus-host disease in bone marrow transplants. (pages 789–794)
The discovery of a family of proteins with strong homology to the uncoupling protein of brown fat has generated great interest as these molecules might represent therapeutic targets for human obesity. Two recent studies have used genetics to explore the role of one of these proteins, UCP2, in the control of mammalian metabolism and come to rather different conclusions.
Recent insights into the receptors expressed by sensory neurons are providing the beginnings of a biological basis for designing therapies to block nociceptive information before it reaches the spinal cord. This approach could potentially avoid some of the side effects in the central nervous system caused by currently available analgesics. (pages 821–826)
The uptake of apoptotic CD40L+ cells by immature dendritic cells leads to dendritic-cell activation. This mechanism might account for the generation of autoreactive CD8+ T cells in HIV infection and indicates a general mechanism for the regulation of autoimmune T-cell responses during infection. (pages 807–813)
Nicotine is widely used as an aid to smoking cessation and is being evaluated to treat non-smoking related disorders. Stimulation of angiogenesis by nicotine raises many questions about its mechanism of action and use in therapy. (pages 833–839)
Mutation is one way in which RNA viruses evade the destructive actions of CD8+ cytotoxic lymphocytes. New research shows that they employ the same method to escape attack by CD4+ T cells. (pages 795–800)
The development of a sensitive in vitro method to amplify the pathological form of the prion protein might provide a tool for the pre-clinical diagnosis of prion diseases.