Cell migration

Lymphocyte transcellular migration occurs through recruitment of endothelial ICAM-1 to caveola- and F-actin-rich domains. Millán, J. et al. Nature Cell Biol. 8, 113–123 (2006)

Vimentin function in lymphocyte adhesion and transcellular migration. Nieminen, M. et al. Nature Cell Biol. 8, 156–162 (2006)

The recruitment of leukocytes from the blood to the tissues requires that they migrate across the endothelium. Although transendothleial migration can occur by both paracellular and transcellular routes, most studies have focused on determining the mechanisms of paracellular migration. However, two studies published in Nature Cell Biology now analyse the mechanisms of transcellular transendothelial migration. Anne Ridley and colleagues observed that when T cells interacted with endothelial cells, the T cells extended protrusions into the endothelial cells at F-actin- and caveolin 1-enriched regions. Furthermore, T cells undergoing transcellular transendothelial migration were surrounded by caveolin 1, F-actin and intercellular adhesion molecule 1 (ICAM1). Importantly, reducing the level of expression of caveolin 1 resulted in a dose-dependent decrease in transcellular transendothelial migration. By contrast, Sirpa Jalkanen and colleagues showed that when peripheral-blood mononuclear cells (PBMCs) and endothelial cells interact, vimentin intermediate filaments from both cells form a complex, highly dynamic network that anchors the cellular adhesion molecules. This network was found to be important for transcellular transendothelial migration; vimentin-deficient PBMCs showed a decreased ability to cross endothelial cells in vitro and to home to mesenteric lymph nodes and the spleen. These data define two molecular pathways by which transcellular transendothelial migration can occur and future studies will be required to determine whether these processes are connected or independent.

Neuroimmunology

Immune cells contribute to the maintenance of neurogenesis and spatial learning abilities in adulthood. Ziv, Y. et al. Nature Neurosci. 9, 268–275 (2006)

Boosting your immune system might boost your brain power. Autoimmune T cells, which are present in healthy individuals, are known to promote neuronal survival and renewal following injury to the central nervous system (CNS), and Michal Schwartz and colleagues propose that this might reflect a normal, homeostatic role for T cells in adult neurogenesis (and therefore learning and memory). After 6 weeks, normal rats that were housed in enriched environments showed a greater degree of neurogenesis than rats that were housed in standard cages, but this natural increase in neurogenesis by environmental stimulation did not occur in immunodeficient mice. Furthermore, genetically engineered mice with an excess of T cells specific for a CNS autoantigen showed both increased neurogenesis and improved learning and memory in water-maze tests compared with their wild-type counterparts.