495 Vitamin A deficiency alters the balance of innate immune cells in the gut, promoting resistance to nematode infection.
http://www.sciencemag.org/content/343/6169/432.abstract
494 The intracellular sensor that triggers the death of human lymphoid CD4 T cells abortively infected with HIV is identified.
http://www.sciencemag.org/content/343/6169/428.abstract
493 Quiescent CD4 T cells in lymphoid tissues are shown to die after HIV-1 infection by caspase-1-mediated pyroptosis, a highly inflammatory form of programmed cell death; caspase 1 inhibitors, which are safe for human use, can rescue the cell death in vitro raising the possibility of new therapeutics targeting the host instead of the virus.
http://www.nature.com/nature/journal/v505/n7484/full/nature12940.html
492 The analysis of multiple SIV vaccine regimens in macaques leads to the identification of a key two-amino-acid signature that confers resistance to neutralizing antibodies; a similar mechanism of immune escape is shown to operate in HIV and may explain the limited efficacy seen in HIV vaccine trials.
http://www.nature.com/nature/journal/v505/n7484/full/nature12893.html
491 Activation of Gpr109a, Receptor for Niacin and the Commensal Metabolite Butyrate, Suppresses Colonic Inflammation and Carcinogenesis.
http://www.cell.com/immunity/abstract/S1074-7613(13)00564-5
490 Induction of Innate Lymphoid Cell-Derived Interleukin-22 by the Transcription Factor STAT3 Mediates Protection against Intestinal Infection.
http://www.cell.com/immunity/abstract/S1074-7613(13)00555-4
489 Sphingolipids from a Symbiotic Microbe Regulate Homeostasis of Host Intestinal Natural Killer T Cells.
http://www.cell.com/abstract/S0092-8674(13)01528-6
488 Premature Activation of the SLX4 Complex by Vpr Promotes G2/M Arrest and Escape from Innate Immune Sensing.
http://www.cell.com/abstract/S0092-8674(13)01545-6
487 Aberrant activation of human TH9 cells may contribute to inflammatory diseases of the skin.
http://stm.sciencemag.org/content/6/219/219ra8.abstract
486 Negatively charged immune-modifying microparticles bind to the scavenger receptor MARCO on inflammatory monocytes, resulting in their apoptosis and reduced inflammatory damage in a range of diseases.
http://stm.sciencemag.org/content/6/219/219ra7.abstract
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