Volume 11 Issue 4, April 2010

Although the life sciences promise huge benefits, the possibility of doing harm from deliberate misuse of knowledge is an increasingly worrisome issue. Discussion and mitigation of these risks by life scientists must be encouraged.

The ability of natural killer cells to eliminate abnormal cells has been shown to be enhanced by triggering of certain inhibitory receptors during their maturation. New data show that sometimes the opposite can happen.

The mechanisms that enforce T cell quiescence are incompletely understood. Slfn2 has now been identified as another participant in this process, functioning as a critical regulator of T cell– and monocyte-mediated immunity.

Neutrophils and other cells secrete the pentraxin PTX3, which promotes innate immunity by binding to pathogens and activating complement. PTX3 can also limit neutrophil recruitment by inhibiting rolling on P-selectin in inflamed venules.

The cross-priming of antigen-specific CD8⁺ T cells requires help. The mechanism by which natural killer T cells provide such help is now characterized.

Surveillance for blood-borne pathogens by immune cells occurs chiefly in the spleen and liver. Kubes and colleagues show that liver Kupffer cells directly sample the bloodstream and are the predominant antigen-presenting cell for invariant natural killer T cells

How and where invariant natural killer T cells encounter glycolipids in vivo remains unclear. Batista and colleagues use multiphoton microscopy to show that CD169⁺ macrophages present lipid antigens to invariant natural killer T cells in lymph nodes.

Dendritic cells classically require cognate licensing by helper T cells to cross-prime cytotoxic T cells. Kurts and colleagues have found an alternative mechanism of cognate licensing mediated by natural killer T cells.

The importance of natural killer cell 'licensing' in vivo remains unclear. Lanier and co-workers now report that 'unlicensed' natural killer cells are more protective than 'licensed' cells during viral infection.

Leukocytes enter inflamed tissues by initiating selectin-dependent rolling on reactive endothelia. Mantovani and colleagues show that the long pentraxin PTX3 competes for P-selectin and acts to limit neutrophil extravasation.

Quiescence must be actively maintained in cells of the immune response. Beutler and colleagues describe a new mutant mouse, elektra, with defective control of T cell and monocyte quiescence; this defect maps to Slfn2.

The mechanism of T cell avidity maturation has remained elusive. Geisler and co-workers show that induction of the phospholipase PLC-γ1 via the alternative p38 pathway is required for avidity maturation in naive human T cells.

The immunological mechanisms of diabetes onset in NOD mice are poorly characterized. Unanue and co-workers find that insulin peptide–reactive (but not insulin protein–reactive) type B T cells can cause diabetes.