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In this issue, Epstein and colleagues show that histone deacetylase 2 (Hdac2) regulates cardiac hypertrophy by modulating the activity of Gsk3β. The cover shows Hdac2 immunostaining (red) in the heart of an E11.5 mouse embryo.
Uneasy with information websites policed by people with little expertise, scientists are creating their own online encyclopedias. But are they accessible enough to supplant Wikipedia, asks Brandon Keim.
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.
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).
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).
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.
Scientists studying tuberculosis are struggling with scarce funds, layers of bureaucracy and a lack of markers that can clearly identify which treatments are working, reports Apoorva Mandavilli.
With a life dedicated to underserved populations from New York to the farthest corners of Africa, Wafaa El-Sadr has earned a reputation among her colleagues as the closest thing to a saint they'll ever meet.
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?
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.
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.
In what direction is the field of tuberculosis going? By bringing together input from top scientists, analysts and decision makers interested in tuberculosis research, this focus identifies the recent papers with the most impact in the discipline and identifies the key issues that are shaping our thinking in this field.