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.
Regulatory T cells are known for their ability to tame the immune response. A molecule has now been identified that can sensitize T cells to this suppressive activity. The findings open the door to new ways of modulating immunity (pages 1088–1092).
The human gastric bacterium Helicobacter pylori can acquire cholesterol from its host and enzymatically alter the molecule to counteract the immune system. The finding reveals yet another strategy used by successful microbial colonizers to evade immunity. Do such strategies make the microbe more like us (pages 1030–1038)?
A mechanism that may underlie a form of human kidney failure has been delineated in knockout mice. Activation of the oxygen-regulated transcription factor Hif1 and its target gene Cxcr4 leads to increased cell proliferation that interferes with the function of the glomerulus (pages 1071–1077).
Circulating natural killer cells might be best known for their ability to disable and maim target cells. But in the pregnant uterus of humans these cells seem to have a positive effect, regulating placental development and angiogenesis (pages 1065–1074).
Treating stroke with tissue plasminogen activator (tPA) can help dissolve blood clots and improve outcome. But tPA also increases the risk of hemorrhage and has other deleterious effects. A new approach to treatment minimizes these negative effects.
Mast cells are thought to contribute to anaphylaxis and damage after snake bites and bee stings. But it now seems that these cells instead mount a defense against venom and inactivate toxins.
Metastatic disease is the primary cause of death for most cancer patients. Complex and redundant pathways involving the tumor cell and the microenvironment mediate tumor invasion at the primary site, survival and arrest in the bloodstream, and progressive outgrowth at a distant site. Understanding these pathways and their dynamic interactions will help identify promising molecular targets for cancer therapy and key obstacles to their clinical development.
Transplantation of metastatic melanoma cells into zebrafish embryo disrupts development—and identifies a potential new drug target for this deadly cancer (pages 925–932).
The key developmental regulator Notch was first characterized in flies but has since been implicated in diseases ranging from cancer to migraine. Experiments in a rat model now suggest that activation of Notch can also promote neurogenesis and healing after stroke.
Certain antibiotics prompt Streptococcus pneumoniae to take up DNA from the environment, which may enable the microbe to acquire genes for antibiotic resistance.
Tyrosine kinase inhibitors, widely hailed for their success as treatments for cancer, are also plagued by the issue of cardiotoxic side effects. The mechanism behind the heart damage now comes to light for one such inhibitor, imatinib mesylate, also known as Gleevec (pages 908–916).
The role of inflammatory mechanisms in amyotrophic lateral sclerosis is a hotly debated topic. Findings in a mouse model now add weight to arguments that targeting of inflammatory cells might be a fruitful therapeutic approach.
Controlling the growth of cancer cells at metastatic sites is one goal of cancer drug development. Studies of metastasis suppressor function bring this long-sought goal closer (pages 933–938).
