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Granulysin, a powerful cytolytic protein secreted from immune cells, underlies an extreme and deadly response to common medications, in which the skin blisters and sloughs off. The findings may also have implications for bone marrow transplant recipients suffering from graft-versus-host disease (pages 1343–1350).
Interfering with the adhesion of immune cells to the cerebral vasculature holds seizures in check, potentially opening a new realm of therapeutics (pages 1377–1383).
A small peptide eases pain in several types of mouse models. The peptide targets a protein interaction within a pain-mediating complex—containing the N-methyl-D-aspartate receptor—without affecting normal physiological processes (pages 1325–1332).
The phosphoinositide 3-kinase (PI3K) and RAS oncoproteins are activated in many major tumor types and control linked signaling pathways. An inhibitor of PI3K is now shown to shrink tumors in transgenic mouse cancer models. The drug also blocks RAS-induced lung tumors when combined with an inhibitor of mitogen-activated protein kinase kinase (pages 1351–1356).
Findings in a mouse model of multiple sclerosis highlight the contribution of CD8+ T cells, previously largely ignored in this disease. The work also helps answer why certain variants of the human leukocyte antigen (HLA) complex are protective, while others increase risk for disease (pages 1227–1235).
The immune system's response to a latent and ubiquitous virus is harnessed to kill tumors in a small study of humans. The approach overcomes a major barrier to effective tumor immunotherapy—generating a sustained immune response (pages 1264–1270).
A small interfering RNA has been engineered to silence an oncogene and activate the immune response simultaneously. The approach shrinks tumors in mice (pages 1256–1263).
Two recent studies—one in humans by Levine et al. in 2004 and one in mice by Venkatesha et al. in 2006—have shown an important role for placental-derived soluble antiangiogenic factors as mediators of the pathologies associated with preeclampsia. These findings may have profound implications for the diagnosis, treatment and prevention of this devastating condition.
A method using tissue engineering principles for the culture of immature ovarian follicles followed by fertilization of oocytes in vitro has been presented by Xu et al.1. This methodology is a great step forward toward new technology for fertility preservation in female cancer patients.
Natural killer (NK) cells, originally so named because they have the capacity to kill other cells without activation, can be licensed and educated to regulate tissue homeostasis. This notion has recently been shown in reproduction—in both normal physiology by Hanna et al. and severe pathophysiology (preeclampsia) by Hiby et al.
Defective signaling of vascular endothelial growth factor seems to underlie the development of hemangiomas, disfiguring tumors arising early in life (pages 1236–1246).
Results from two independent groups of researchers have revolutionized our thinking about the potential long-term consequences of exposure to common foreign chemicals, or xenobiotics. The studies indicate that exposure to such chemicals during key windows of gestation can affect not only the children exposed in utero but also their children and perhaps even their grandchildren.
Although it has been thought that female mammals develop all the eggs they will ever have by the time they are born, new research suggesting otherwise has now sparked a debate.
Producing germ cells in vitro would open important new avenues for regenerative medicine, and obtaining alternative sources of pluripotent stem cells is desirable. In this regard, Geijsen et al. have shown that it is possible to differentiate stem cells into cells similar to male gametes, whereas Guan et al. reported the ability to turn undifferentiated germ cells into pluripotent stem cells.
A small number of women (approximately 1%) suffer from premature ovarian failure in which their ovarian follicle reserve is exhausted before age 40. Recent studies in mice show that the absence of a tumor suppressor gene, PTEN, in oocytes prematurely induces global follicular activation, depleting the follicle reserve in a manner similar to premature ovarian failure.
Comparative studies of the immune response to simian immunodeficiency virus in two nonhuman primate species provide insight into a central aspect of HIV infection—the ability of the virus to cause chronic activation of the immune system (pages 1077–1087).
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).
