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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 cytidine deaminase AID is required for antibody gene diversification. Casali and colleagues show that the transcription factor HoxC4 is expressed in germinal centers and is required for AID expression.
Foxo transcription factors influence a wide variety of cellular responses. Hedrick and colleagues show that dendritic cells express Foxo3 to suppress the production of interleukin 6 and prevent excessive accumulation of antigen-specific T cells.
Several NOD2 mutations are associated with a greater risk of Crohn's disease. Ma and colleagues show that the 3020insC Nod2 mutant actively suppresses IL10 transcription by interfering with phosphorylation of the nuclear ribonucleoprotein hRNP-A1.
The functions of individual dendritic cell subsets in the skin are unclear. Heath and colleagues now show that langerin-positive CD103+ dermal dendritic cells are the main migratory subtype able to cross-present antigen.
T cell antigen receptor signaling occurs in microclusters that coalesce into immune synapses. Bretscher and colleagues show that myosin IIA is required for directed microcluster movement and sustained T cell antigen receptor signaling.
Inhaled allergens induce many changes in airway function. Kheradmand and colleagues show that matrix metalloproteinase 7 activates the cytokine interleukin 25 and inhibits retinoic acid–mediated induction of regulatory T cells, thereby heightening allergic responses.
Whether TH1 or TH-17 cells initiate experimental autoimmune encephalomyelitis is unclear. Sallusto and colleagues now show that CCR6+ TH-17 lymphocytes initiate it by entering the brain through the choroid plexus.
MHC class I presentation of viral peptides aids CD8+ T cell recognition of infected cells. Desjardins and colleagues describe an MHC class I viral peptide presentation pathway that integrates autophagosomes and proteasome-dependent processes.
The relationship between peripheral and recirculating memory cells remains mostly undefined. Carbone and colleagues present evidence of tissue-resident memory T cells that can provide protective immunity at points of pathogen entry.
In peripheral lymphoid organs, γδ T cells are a source of interleukin 17. Silva-Santos and colleagues find that production of interleukin 17 versus interferon-γ by γδ T cells is inflexible and is determined in the thymus.
Toll-like receptors (TLRs) induce complex transcriptional responses. Aderem and colleagues use systems-biology approaches to show that three transcription factors, NF-κB, ATF3 and C/EBPδ, work together to distinguish persistent versus transient TLR stimuli.
The function of the CD98hc transmembrane protein in adaptive immune responses has been unclear. Ginsberg and colleagues show that CD98hc is needed for B cell proliferation and subsequent plasma cell differentiation.
Lymphocytes are typically recruited into lymph nodes via CCR7. Gunn and colleagues identify an 'inflammatory DC' subset that is recruited directly from the bloodstream through the use of CCR2 and that induces potent T helper type 1 priming.
High-affinity isotype-switched B cells arise in germinal centers. Locksley and colleagues show that follicular helper T cells are the main cytokine providers for GC B cells and thereby directly influence the ensuing antibody response.
Efficient humoral immunity requires B cell–T cell interactions in lymphoid follicles. McHeyzer-Williams and colleagues show that CXCR5+ follicular helper T cells have T cell antigen receptors with higher affinity for antigen than do other responding effector helper T cells.
The molecular mechanisms that govern B cell progenitor localization in bone marrow sinusoids are not understood. Cyster and colleagues demonstrate involvement of cannabinoid receptor 2 in retaining developing B cells in sinusoids.