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Certain oncogenes seem to be able to trigger cellular senescence and growth arrest, thereby holding cancer at bay. Two new studies suggest that oncogenes trigger senescence through activation of a pathway initially described as sensing DNA damage.
A protein has been identified that promotes the formation of osteoclasts, bone-degrading cells—while also inhibiting osteoblasts, bone-forming cells. The findings could lead to new avenues of drug development to strengthen bone (pages 1403–1409).
An explanation has come to light for the long-observed phenomenon that ultraviolet light suppresses the immune response in the skin. Light and other stimuli prompt the proliferation of regulatory T cells through the upregulation of receptor activator of NF-κB ligand (RANKL) on skin cells (pages 1372–1379).
HIV-1 infection results in chronic activation of the immune system—a process that is thought to contribute to T-cell depletion and progression to AIDS. Chronic activation is now suggested to occur through a breakdown of the mucosal barrier and stimulation of immune cells by microbial products (pages 1365–1371).
Dietary lipids seem to activate a Toll-like receptor, which is better known for its defense against infectious pathogens. The findings suggest that the resulting inflammatory response may link obesity with type 2 diabetes.
Activation of certain G protein–coupled receptors stimulates production of the neurotoxic amyloid-β peptide through internalization of a membrane-embedded protease (pages 1390–1396).
The goal of replacing dying cells in Parkinson disease with stem cells is now brought a step closer to the clinic. A new protocol eases symptoms in a rat model of the disease, but also raises the concern that poorly differentiated cells have the potential to become tumorigenic (pages 1259–1268).
A molecular basis for the metabolic abnormalities observed in Huntington disease is emerging. Transcription of a key mitochondrial regulator, PGC-1α, is dysregulated by mutant huntingtin, leading to oxidative stress and excitotoxicity. The findings dovetail with previous work implicating aberrant transcription in Huntington disease, and have implications for related conditions such as Parkinson disease.
Blockade of a single cytokine—interleukin-10—can re-energize T cells 'exhausted' by persistent virus infection. The findings have implications for controlling HIV and other persistent viruses (pages 1301–1309).
Thickening of the cardiac valves leads to congestive heart failure, chest pain, sudden loss of consciousness and often death. Experiments in mice now link this condition to dysregulation of an endogenous inhibitor of angiogenesis (1151–1159).
HIV causes a chronic infection that overwhelms the immune system and leads to T-cell exhaustion. Three groups now report that a signaling molecule that dampens immune responses may tucker out the T cells (1198–1202).
Presenilins are thought to contribute to Alzheimer disease through a protein cleavage reaction that produces neurotoxic amyloid-β peptides. A new function for presenilins now comes to light—controlling the leakage of calcium out of the endoplasmic reticulum. Is this a serious challenge to the 'amyloid hypothesis' of Alzheimer disease?
A variant gene for antigen presentation is associated with tissue damage in multiple sclerosis. The damaging effects are now shown to be dampened by an allele of a second, neighboring gene.
Many individuals with chronic myeloid leukemia have benefited from the drug imatinib (Gleevec)—but if they are taken off the drug, relapse occurs. Two mathematical models to explain this phenomenon, one described in this issue, have come to different conclusions (1181–1184).
