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A single molecule, osteopontin, seems to both amplify and quell the immune response in asthma—depending on the stage of the asthmatic reaction. The findings hint that, if given at the right stage, osteopontin might have value as a therapy (pages 570–578).
A drug that elevates host cAMP levels forces pathogenic bacteria out of bladder epithelial cells. This process may make urinary tract infections more amenable to treatment with antibiotics (pages 625–630).
The presence of autophagic morphology in failing heart muscle cells has suggested that autophagy causes heart failure. Instead, it seems that the opposite is true: autophagy is critical for normal heart function (pages 619–624).
Activation-induced cytidine deaminase (AID), which mediates antibody diversification, is now implicated as an inducer of p53 mutagenesis in cancer cells (pages 470–476).
Chemokines in the brain recruit immune cells from the blood or from within the brain. Disrupting this line of communication exacerbates disease in mouse models of Alzheimer disease (pages 432–438).
Platelets act as intermediaries in the pathogenesis of sepsis—sensing bacteria and signaling neutrophils to release fibrous traps that remove bacteria from the bloodstream. This response may also contribute to tissue injury (pages 463–469).
Findings from a mouse model of multiple sclerosis suggest that regulatory T cells alone cannot outduel pathogenic T cells in the central nervous system. The observations may have implications for experimental approaches designed to dampen autoimmune diseases by infusion of regulatory T cells (pages 423–431).
'Impulsivity' occurs frequently in people with addiction and other common disorders such as attention deficit hyperactivity disorder (ADHD). Experiments in rats suggest that reduced dopamine receptor availability in the brain's ventral striatum may underlie links between impulsivity and addiction.
New classes of chemical compounds along with more efficient methods to identify drug targets have produced exciting developments in antituberculous antibiotics. Will the new drugs now entering clinical trials have an impact on treatment?
Modulation of events regulated by α2-adrenergic receptors counteracts heart failure by restoring proper signaling from the adrenal gland to the heart (pages 315–323).
A promising experimental vaccine strategy, just entering clinical trials, displays a deleterious effect in mice. Use of antibodies to CD40 seems to clamp down on the long-term ability of T cells to respond to antigen (pages 354–360).
Identification of drug targets in M. tuberculosis is a challenge for bench science. High-throughput mutagenesis with transposons together with microarray-based genome and transcriptome profiling has begun to meet this challenge.
Persistence of Mycobacterium tuberculosis in humans depends on its ability to survive within the host macrophage. So the bacterium must resist antimicrobial mechanisms or subvert macrophage signaling pathways to prevent its death. Recent evidence suggests that the two strategies are not mutually exclusive.
Langerhans cells in the skin and mucosa have been thought to mediate the spread of HIV-1 in the body during sexual transmission. Instead, it seems that the cells protect against the virus, a finding with implications for the development of microbicides (pages 367–371).
