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.
During infections, Mycobacterium tuberculosis has to acquire nutrients and resist host defense. Lipids are important for both: host-derived lipids provide food, whereas pathogen-derived lipids mediate immune suppression.
The genomic region lost during the attenuation of BCG vaccine encodes a newly discovered secretion system conserved among gram-positive bacteria. A series of papers has now dissected the components of this system, revealing a unique Mycobacterium tuberculosis–specific signal for export of bacterial proteins into the host.
Psoriasis results from cross-talk between immune cells and keratinocytes in the skin. The nature of these signals now comes to light, revealing potential roles for IL-23 and a TH17 response.
Regulatory T cells (Tregs) have gone from obscurity to rock-star status in the past decade, prompting intense scrutiny—but what exactly are they? Four studies examine this question, delving deeply into the role of the transcription factor Foxp3 in governing Treg differentiation and function.
An orally available drug enters the brain and interferes with signaling of orexin neuropeptides—providing a potential treatment for sleep disorders and possibly addiction (pages 150–155).
The nuclear hormone receptor LXR—best known for sensing cholesterol metabolites—also responds to glucose. The findings give LXR a central role in modulating the body's response to metabolic inputs.
A drug commonly used to treat high blood pressure shows promise as a treatment in mouse models of Marfan syndrome and muscular dystrophy (pages 204–210).
A new approach to treating leaky blood vessels emerges from a proteomic analysis. The findings have implications for diabetic retinopathy and other diseases associated with increased vascular permeability (pages 181–188).
The ability to visualize brain pathology in living individuals with Alzheimer disease could change how the disease is diagnosed and drugs to treat it tested. A recently developed positron emission tomography tracer helps to image fibrillar amyloid-β and neurofibrillary tangles and brings us closer to this goal.
An inhibitor of the Wnt signaling pathway mediates bone destruction in inflammatory arthritis. The inhibitor may be the key to understanding why in some joint diseases bone is destroyed and in others built up (pages 156–163).
Defects in organelle biogenesis and trafficking underlie a newly described genetic disorder. These defects are traced to the gene encoding a scaffolding protein that coordinates signal transduction events on late endosomes (pages 38–45).
Three studies identify multipotent progenitor cells that can give rise to major cell types of the heart. The findings may lead to improved approaches for heart repair.
Three studies should shift thinking about the causes of inflammatory bowel disease. It seems that researchers have been focusing on the wrong cytokine as a driving force.
The retinoblastoma gene (RB) was the first tumor suppressor gene cloned. But, until recently, little clinical progress had been made to target human tumors deficient in RB function. A new approach emerges from studying retinoblastoma tumors.
