Volume 10 Issue 7, July 2009

It has been 10 years since the first workshop on natural killer T cells helped to launch a growth phase for this field of research.

The US National Institute of Allergy and Infectious Diseases convened a workshop of malaria investigators and immunologists to foster collaborations and attract more immunologists into malaria research. Discussions highlighted research gaps and underscored the incomplete understanding of basic immune mechanisms that contribute to the pathogenesis of or protection against malaria.

Dendritic cells are best known as antigen-presenting cells that initiate adaptive immune responses. Three new papers suggest that basophils initiate allergen- and helminth-driven CD4⁺ T helper type 2 responses by functioning as antigen-presenting cells in draining lymph nodes.

DAP12-coupled receptors influence signals emanating from Toll-like receptors, integrins and receptors for cytokines and growth factors. New findings indicate that DAP12 also facilitates the ability of CSF-1R, the receptor for M-CSF, to induce the stabilization and nuclear translocation of β-catenin.

Deficiency in acid sphingomyelinase causes lysosomal storage of sphingomyelin, mediates resistance to stress-induced apoptosis and alters susceptibility to certain infections. New work links acid sphingomyelinase to the granule exocytosis of cytotoxic T cells.

The receptor for the lipid mediator sphingosine 1-phosphate is critical for T cell trafficking. New data show that signaling mediated by this receptor critically controls the development, maintenance and suppressive activity of natural regulatory T cells that express the transcription factor Foxp3.

Basophils act as effector cells in immunoglobulin E–mediated hypersensitivity responses. Artis, Nakanishi and Medzhitov and their colleagues report that basophils present antigen and induce T helper type 2 responses to helminths, allergens and immunoglobulin E immune complexes.

Basophils act as effector cells in immunoglobulin E–mediated hypersensitivity responses. Artis, Nakanishi and Medzhitov and their colleagues report that basophils present antigen and induce T helper type 2 responses to helminths, allergens and immunoglobulin E immune complexes.

Basophils act as effector cells in immunoglobulin E–mediated hypersensitivity responses. Artis, Nakanishi and Medzhitov and their colleagues report that basophils present antigen and induce T helper type 2 responses to helminths, allergens and immunoglobulin E immune complexes.

Complement forms an ancient innate immune defense. Gros and colleagues provide new insight into the interactions between complement convertase C3b and its regulator factor H and with the staphylococcal inhibitor SCIN.

Complement forms an ancient innate immune defense. Gros and colleagues provide new insight into the interactions between complement convertase C3b and its regulator factor H and with the staphylococcal inhibitor SCIN.

Macrophage colony-stimulating factor (M-CSF) induces the proliferation of mononuclear phagocytes, and DAP12 is needed for their function. Colonna and colleagues show that DAP12 is also needed for M-CSF-induced stabilization of β-catenin.

E3 ubiquitin ligases are critical for innate and adaptive immunity. Cao and colleagues show that the E3 ubiquitin ligase Nrdp inhibits the production of proinflammatory cytokines while promoting the release of interferon-β in Toll-like receptor–triggered macrophages.

Immunological synapses (IS) involving surface receptors form between dendritic cells (DC) and T cells. Rodriguez-Fernandez and colleagues show that IS-induced signals activate Akt and NF-κB and suppress Foxo1 to promote DC survival.

Granules containing perforin and granzymes are secreted from cytotoxic T lymphocytes. Krönke and co-workers find that acid sphingomyelase is needed for granule shrinkage just before exocytosis in this process.

Regulatory T cells (T_reg cells) are necessary for maintaining peripheral tolerance. Chi and colleagues show that the receptor S1P₁ negatively regulates thymic T_reg cell production and blocks T_reg cell activity via an Akt-mTor pathway.

How interleukin 17 influences B cell biology is unclear. Bonnefoy-Bérard and colleagues find that interleukin 17 alone or in combination with B cell–activating factor controls the survival, proliferation of human B cells and their differentiation into immunoglobulin-secreting cells.

Immune complexes are captured from lymph by subcapsular macrophages. Cyster and colleagues show that an intricate relay shuttles antigen into germinal centers to drive affinity maturation.