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Host microRNAs control both cellular processes and viral protein translation. Mandelboim et al. demonstrate synergism between host and viral microRNAs in downregulating the activatory ligand MICB, which facilitates immune evasion.
Fish lack immunoglobulin A, which suggests that they lack specialized mucosal antibodies. Sunyer and colleagues show that immunoglobulin T fulfills this mucosal antibody function and engenders protection against gut parasites.
Type 1 regulatory T cells control autoinflammatory diseases. In two linked papers, groups led by Kuchroo and Quintana demonstrate the role of the aryl hydrocarbon receptor in the differentiation of these cells.
Type 1 regulatory T cells control autoinflammatory diseases. In two linked papers, groups led by Kuchroo and Quintana demonstrate the role of the aryl hydrocarbon receptor in the differentiation of these cells.
Immunoglobulin class-switch recombination can be induced by the secreted factors BAFF and APRIL. Cerutti and colleagues show that the receptor TACI conveys such signals via the adaptor MyD88 to induce class-switch recombination.
Activation-induced cytidine deaminase triggers somatic hypermutation and immunoglobulin class switching. Mills and colleagues show that it can also cause widespread mutations outside the immunoglobulin heavy-chain locus.
How Roquin controls expression of the inducible costimulator ICOS remains unclear. Heissmeyer and co-workers now show that Roquin binds to the 3' untranslated region of ICOS mRNA and interacts with proteins that confer post-transcriptional repression.
Integrins regulate the migration of leukocytes in inflammation. Cao and co-workers now show that CD11b is activated by Toll-like receptor–triggered inside-out signaling and feeds back to inhibit phosphorylation of the adaptors MyD88 and TRIF.
RNA-binding proteins are involved in post-transcriptional regulation. Turner and co-workers show that these proteins are also critical in thymopoiesis.
Functional μ-immunoglobulin heavy chains pair with VpreB and λ5 to form precursor B cell antigen receptors. Jumaa and colleagues show that glycosylation at asparagine 46, a unique modification specific to the μ-heavy chain, is required for the function of such receptors.
Virulent Mycobacterium tuberculosis inhibits apoptosis of infected macrophages. Behar and co-workers show that inhibition of apoptosis prevents cross-presentation of M. tuberculosis antigens by dendritic cells and impedes initiation of T cell immunity.
PLZF is known to be a transcription factor for natural killer T cells. Now Hogquist and colleagues demonstrate that PLZF+ T cells regulate the size of the CD8+ memory T cell pool.
Type I interferons (IFN-α and IFN-β) are key to antiviral immunity. Kim and Seed now demonstrate that the transcription factor MAFB acts as a metastable switch to control expression of IFN-β.
Mucosal-associated invariant T cells are evolutionarily conserved innate lymphocytes whose physiological function has remained unclear. Lantz and colleagues now demonstrate an important antimicrobial function for these cells.
Lineage specification and development require a hierarchy of transcription factors. Murre and colleagues have compiled a genome-wide set of cis-acting targets centered on E2A, EBF1 and Foxo1 that govern early B cell development.
The classical model of hematopoiesis proposes an early split of the lymphoid and myeloid lineages. Dick and co-workers show that as in the mouse, human hematopoiesis does not follow a rigid model of myeloid-lymphoid segregation.
Immunoglobulin E–mediated crosslinking of FɛRI receptors can lead to life-threatening anaphylaxis in sensitized people. Shibuya and colleagues identify a phosphatase-recruiting inhibitory receptor, Allergin-1, that suppresses mast cell degranulation induced by immunoglobulin E–FɛRI.
Whether environmental antigens can elicit autoimmunity remains unclear. Goverman and colleagues show that viral infection breaks self-tolerance via activation of CD8+ T cells expressing dual T cell antigen receptors, without bystander activation or molecular mimicry.
Tissue-resident leukocytes migrate to draining lymph nodes after being activated. Kumanogoh and colleagues show that such entry requires semaphorin 3A, produced by lymphatic vessels, to activate plexin-A1 receptors on migrating dendritic cells.
The mechanisms that initiate T helper type 2 responses are poorly understood. Pulendran and colleagues now show that such responses to cysteine proteases require dendritic cell–basophil cooperation via signaling mediated by reactive oxygen species.