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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.
Regulatory T cells (Treg cells) are necessary for maintaining peripheral tolerance. Chi and colleagues show that the receptor S1P1 negatively regulates thymic Treg cell production and blocks Treg cell activity via an Akt-mTor pathway.
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.
The function of interleukin 17 in the pathogenesis of chronic inflammatory disorders is controversial. Flavell and colleagues now demonstrate that interleukin 17A mediates a protective effect on T cell—driven intestinal inflammation in vivo.
Immunoglobulin gene rearrangements occur in an organized, temporal way. Skok and colleagues show that immunoglobulin alleles 'pair' to coordinate cleavage and allelic availability.
The reorientation of the T cell microtubule-organizing center toward the antigen-presenting cell enables the directional secretion of cytokines and lytic factors. Huse and colleagues show that this process depends on diacylglycerol.
How and where bacterial recognition triggers the induction of type I interferon is unclear. Teti and colleagues show that phagosomal bacteria trigger Toll-like receptor 7–dependent interferon production in lysosomes of conventional dendritic cells.
The function of T cell antigen receptor (TCR) specificity in thymic regulatory T cell development is controversial. Hsieh and colleagues show that this development is a 'TCR-instructive' process that depends on a small selecting niche
The transcription factor ELF4 controls hematopoietic stem cell quiescence. Lacorazza and colleagues show that ELF4 is also needed to maintain the quiescence of naive T cells during steady-state conditions and after antigen stimulation.
Cytotoxic T lymphocytes recognize a restricted set of immunodominant HIV peptide epitopes. Iversen and colleagues show that the cleavage and abundance of HIV peptides are influenced by intraepitope as well as flanking virus escape mutations.
How transcription factor NF-κB influences B cell development remains enigmatic. Rajewsky and colleagues show that NF-κB activation driven by the kinase IKK is required for the generation of B cells expressing immunoglobulin-λ but not immunoglobulin-κ light chains.
Toll-like receptor signaling must be carefully regulated to avoid excessive inflammation. O'Neill and colleagues identify a splice variant of the adaptor TRAM that negatively regulates MyD88-independent pathway activated by Toll-like receptor 4.
Several subsets of Foxp3+ regulatory T cells are known to exist. Campbell and colleagues show that one subset of regulatory T cells requires the transcription factor T-bet during T helper type 1–mediated immune responses in vivo.
The 3020insC mutation in Nod2 is associated with Crohn's disease, but how it influences disease pathogenesis is unknown. A new study shows that the 3020insC mutant protein fails to activate a key transcription factor that drives interleukin 10 expression, resulting in reduced production of this anti-inflammatory cytokine.
T cell expansion and contraction during the immune response to pathogens are regulated by a wide variety of cell-intrinsic and cell-extrinsic factors. A new study identifies a role for CTLA-4 signaling and activation of the Foxo3 transcription factor in modulating T cell populations.