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MicroRNAs contribute to HIV-1 latency in resting T cells. This finding could potentially be used in the development of therapies targeted to purge the latent reservoir in an effort to clear the body of virus (pages 1241–1247).
Cytokine signaling from the tumor microenvironment can allow leukemia cells to survive targeted imatinib therapy, in the first report of a non-autonomous resistance mechanism.
The innate and adaptive immune systems act in concert to effectively combat infection while minimizing collater al damage caused by the host immune response. T cells of the adaptive immune system have now been shown to suppress overzealous early innate responses to infection that can lead to 'cytokine storm'–mediated death (pages 1248–1252).
The S6K1 kinase lies downstream of a signaling network crucial for muscle hypertrophy. It now seems that S6K1 also interacts with another kinase—AMPK—to integrate muscle-cell growth with metabolic regulation.
In the inherited anemia β-thalassemia, diseased red blood cell precursors release a blood-borne signal that promotes excessive intestinal iron absorption, predisposing affected individuals to multiorgan damage (pages 1096–1101).
A drug that activates glutamate receptors offers promise for a new class of anti-psychotic therapeutics and sheds light on the pathophysiology of this devastating disease (pages 1102–1107).
Oxidized products of low-density lipoproteins (LDLs) activate platelets through CD36, demonstrating a link between deregulated lipoprotein levels, oxidative stress and thrombosis (pages 1086–1095).
The bone-specific protein osteocalcin has now been shown to act as a hormone that profoundly affects glucose and fat metabolism. This discovery completes an endocrine circuit with the skeleton as a ductless gland.
T cells attack Plasmodium-infected hepatocytes when fighting malaria, and it was thought that T cells first encountered Plasmodium antigens in the liver. Instead, immediately after infection, small numbers of parasites drain to skin lymph nodes where they can prime T cells to mount a protective immune response (pages 1035–1041).
The role of microbial pathogens in human cancer is a fertile area of research, with important implications for treatment. Two pathogens implicated in Burkitt's lymphoma have now been shown to directly interact with one another.
A genetic lineage-tracing study provides evidence that adult progenitor cells repopulate the cardiomyocyte pool in diseased hearts, but not during normal aging (pages 970–974). These stem cells could become the basis for innovative ways to treat or prevent heart failure.
Mice deficient for the cytokine interleukin-15 are unexpectedly protected from sepsis. Orinska and colleagues show that interleukin-15 signals intracellularly in mast cells and limits their recruitment of neutrophils to clear the infection (pages 927–934).
Cyclin-dependent kinase 5, a serine/threonine kinase, contributes to neurodegeneration in Parkinson's disease. This kinase is now shown to phosphorylate peroxiredoxin-2, inactivating it, and thereby sensitizing neurons to the deleterious effects of parkinsonian toxins.
Contemporary M1 strains of Streptococcus pyogenes have acquired a DNase gene that improves the virulence of the bacterium, but its expression is repressed by the CovRS regulatory system. Walker et al. report that the bacteria are under selective pressure to mutate the covRS locus to maintain DNase expression for invasive infection (pages 982–986).
Rosacea is a common skin disorder marked by chronic inflammation and vascular abnormalities. Two new features of the skin lesions have been identified: elevated levels of cathelicidin antimicrobial peptides and of a related serine protease. These molecules of innate immunity may represent key elements of pathogenesis, as well as new targets for effective therapies (pages 975–981).
