News & Views in 2003

Autoimmunity is suspected to contribute to the formation of atherosclerotic plaques. Studies in mice suggest that this response may instead be protective—and that it may be enhanced with a vaccine (pages 736–743).

Is diabetes a disease of the central nervous system? New data point in that direction. Alterations of the levels of long chain fatty acids in the hypothalamus are now shown to influence glucose homeostasis (pages 756–761).

T cells are recruited into the battle against pathogens by interaction with professional antigen-presenting cells (APCs). A new study shows that this recruitment phase is short and terminates when newly activated T cells kill the activating APCs.

Expressing pancreatic transcription factors in the liver drives the formation of insulin-producing cells and normalizes blood glucose levels in a mouse model of diabetes (pages 596–603).

The evaluation of drug combinations for cancer treatment has progressed slowly through methodical clinical research. A new study examining gene expression profiles could signal a shift in the approach to combination therapy.

Three new studies examine how a regulator of calcium homeostasis contributes to heart failure in humans and mice.

Cells of the innate immune system get energy almost entirely from glycolysis, enabling survival under a variety of harsh conditions. The transcriptional regulator HIF-1 is now placed at the center of metabolic control in these cells.

Epigenetic suppression of FANCF, a member of the Fanconi anemia gene family, is now implicated in some ovarian cancers. Might this suppression explain the sensitivity of such cancers to the cross-linking agent cisplatin (pages 568–574)?

Restoration of genes lost during the original attenuation of the commonly used BCG tuberculosis vaccine enhances the ability of a recombinant strain to protect against Mycobacterium tuberculosis.

Transplantation carries the risk of Kaposi sarcoma, which afflicts 1 out of 200 transplant recipients in the United States. An analysis of human post-transplant tumors indicates that the disease can originate from donor cells, highlighting the need for organ pre-screening.

HIV-1 readily mutates to escape the immune response, evolving in ways that allow it to persist in the host. New findings reveal that HIV-1 protects itself from antibodies by putting up a shield of constantly shifting sugar moieties. This shield may be contributing to the poor performance of candidate HIV-1 vaccines.

Osteopetrosis, a disease characterized by dense bones, is now pinned to the same gene that underlies a coat-color defect in mice (pages 399–406).

A new model addresses the evolutionary mechanisms for antibiotic resistance and comes up with some grim forecasts. In the United States, resistance of Streptococcus pneumoniae to two commonly prescribed antibiotics is predicted to reach 41% by 2004 (pages 424–430).