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Immunity-related GTPase 1 (Irgm1) is needed for defense against bacteria that reside in phagosomes of macrophages. MacMicking and colleagues identify molecular mediators that act 'upstream' and 'downstream' of Irgm1 in the phagosomal membrane.
After binding double-stranded RNA, RIG-I induces production of type 1 interferon. Hornung and colleagues find that RIG-I detects viral DNA via double-stranded RNA intermediates generated by RNA polymerase III.
The molecular mechanisms that underpin thymocyte selection remain incompletely defined. Groups led by Love, Gascoigne and Schwartz independently identify Themis, a signaling protein essential for the positive selection of thymocytes.
Apoptosis of Mycobacterium tuberculosis (Mtb)-infected macrophages restricts the spread of infection. Basu and colleagues delineate the signaling pathway needed for death of Mtb-infected cells.
The molecular mechanisms that underpin thymocyte selection remain incompletely defined. Groups led by Love, Gascoigne and Schwartz independently identify Themis, a signaling protein essential for the positive selection of thymocytes.
The molecular mechanisms that underpin thymocyte selection remain incompletely defined. Groups led by Love, Gascoigne and Schwartz independently identify Themis, a signaling protein essential for the positive selection of thymocytes.
Helper T cells become polarized to effect a 'division of labor'. Sallusto and Spits and colleagues identify a new subset of skin-homing helper T cells, TH-22 cells, that secrete interleukin 22.
Helper T cells become polarized to effect a 'division of labor'. Sallusto and Spits and colleagues identify a new subset of skin-homing helper T cells, TH-22 cells, that secrete interleukin 22.
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.
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.
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.
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.
Tonic antigen receptor signaling contributes to the homeostasis of naive lymphocytes. Alarcón and colleagues show that resting lymphocytes transmit tonic antigen receptor signals through the GTPase TC21 to trigger the PI(3)K pathway.
Mature B cells express immunoglobulin D, but its function is unknown. Cerutti and colleagues show that respiratory mucosal B cells secrete immunoglobulin D, which activates basophils and enhances antimicrobial function.
Macrophages infected with virulent Mycobacterium tuberculosis die by necrosis. Remold and colleagues show that virulent M. tuberculosis promotes necrosis by damaging the plasma membrane and inhibiting its repair.
Mouse strains show varying inherent biases to T helper type 2 (TH2) responses. Bix and colleagues identify Mina, a jumonji C protein, as a negative regulator of the gene encoding interleukin 4 whose expression inversely correlates with TH2 bias.