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Infections with fimbriated bacteria may trigger autoimmunity and cause a form of severe vasculitis that affects capillaries in the kidney and that can destroy the organ (pages 1088–1096).
For years, researchers have debated whether the enzyme lipoprotein-associated phospholipase A2 (Lp-PLA2), produced by inflammatory cells, is a 'good guy' or 'bad guy' in atherosclerosis. Work in pigs provides strong support for the view that Lp-PLA2 promotes the formation of atherosclerotic lesions and dangerous, unstable atherosclerotic plaques (pages 1059–1066).
Upregulation of a protein involved in lysosomal degradation of proteins helps stave off some of the cellular decline observed with aging. The findings could lead to new approaches to fend off age-related disease or even extend lifespan (pages 959–965).
A relatively obscure immune cell, the eosinophil, has a dramatic way of defending against pathogens. It rapidly ejects mitochondrial DNA, ensnaring bacteria and hastening their demise (pages 949–953).
Investigation of a genetically attenuated malaria parasite—which infects but does not kill its host—provides insight into how to develop a malaria vaccine (pages 954–958).
Extracellular DNA floating around in blood plasma provides an accessible template for detecting mutations associated with tumors. A new technique is able to quantify such mutated DNA and predict relapse in individuals with colorectal cancer. The technique complements other approaches, such as the analysis of tumor cells in the plasma (pages 985–990).
Women with pre-eclampsia, a potentially deadly complication of pregnancy, produce agonistic autoantibodies against angiotensin receptor-1, a transmembrane protein that regulates blood pressure. Findings in mice suggest how these antibodies might help trigger the condition (pages 855–862).
A large multicenter study shows that lung adenocarcinomas have messenger RNA expression signatures that greatly add to the use of clinical data in predicting an individual's survival (pages 822–827).
One of the body's key defenders against infection—the activated macrophage—engulfs bacteria and destroys them with an acid cocktail inside lysosomes. Mycobacterium tuberculosis seems to have evolved a strategy to cope with this threat (pages 849–854).
The most effective drug to treat acute ischemic stroke, tissue plasminogen activator (tPA), must be applied within three hours after symptom onset because of the risk of hemorrhage and other complications such as neurotoxicity. The anticancer drug imatinib (Gleevec) may help overcome these limitations by counteracting the ability of tPA to increase the permeability of the blood-brain barrier (pages 731–737).
Two commonly prescribed drugs, statins and aminobisphosphonates, may be helpful in combating the rare aging disorder, Hutchinson-Gilford progeria syndrome (pages 767–772).
Gallstone disease occurs more frequently in subjects with the metabolic syndrome and type 2 diabetes. Findings in a mouse model suggest that the forkhead transcription factor FoxO1 lies behind this association (pages 778–782).
In 1974, Gilbert Ashwell and Anatol Morell discovered a receptor in the liver that recognizes particular glycoproteins, dubbed asialoglycoproteins. We asked Ashwell about his discoveries and what he thinks of the study by Grewal et al.1 in this issue, which suggests that the receptor is involved in regulating sepsis.
A new layer of gene regulation emerges for the metabolic regulator peroxisome proliferator–activated receptor-δ (PPAR-δ). A team consisting of a Krüppel-like transcription factor and a SUMO protease regulate the expression of PPAR-δ target genes, thereby controlling energy metabolism (pages 656–666).
Infectious agents can induce inflammatory lung disease akin to asthma and chronic obstructive pulmonary disease. Work in a new mouse model provides mechanistic insight into this process and uncovers a key role for invariant natural killer T cells (pages 633–640).
A variety of immune cell types contribute to disease in individuals with multiple sclerosis, an autoimmune condition of the central nervous system. Thomas Prod'homme and Scott Zamvil comment on the 'Bench to Bedside' approach, examining how recent basic research implicates the antigen-presenting cell in this disease. In our 'Bedside to Bench' column, Hans Link explores how recent clinical trials may bolster a mechanistic role for the B cell.
The energy-regulating hormone leptin affects signals emerging from certain brain regions. New results explore the nature of these signals, finding a central role for phosphoinositide-3 kinase in the brain and the endocannabinoid system in adipocytes (pages 667–675).
