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Antibodies can be carried into the cell during pathogen infection. McEwan and colleagues show that recognition of intracellular antibodies by the cytosolic antibody receptor TRIM21 activates immunological signaling (p 327; News and Views by Teunis B.H. Geijtenbeek & Sonja I. Gringhuis, p 309). Artwork by Lewis Long.
Antibodies bound to pathogens that invade cells are sensed in the cytosol by the receptor TRIM21, which triggers innate signaling that leads to protective immunity.
The priming of naive T cells requires antigen presentation by activated dendritic cells, yet the optimal generation of effector and memory CD8+ T cells requires subsequent T cell–T cell interactions during the critical differentiation period.
The conversion of cells of the TH17 subset of helper T cells that previously expressed interleukin 17A (IL-17A) and the transcription factor RORγt into follicular helper T cells is needed to generate antigen-specific immunoglobulin A in gut mucosa, which suggests new connections in the cognate control of regional adaptive immunity.
Persistence is a poorly understood yet widespread outcome of viral infection. A study of RNA viruses in flies now shows that viral fragments endogenized as cDNA during the reverse transcription of retrotransposons provide immunity based on RNA-mediated interference in persistently infected cells.
During pathogen infection, antibodies can be carried into the cell, where they are detected by the cytosolic antibody receptor TRIM21. McEwan and colleagues show that the recognition of intracellular antibodies by TRIM21 activates immunological signaling.
The CARM1–MALT1–Bcl-10 complex links ligation of the antigen receptor to NF-κB activation. Thome and colleagues show that MALT1 paracaspase activity requires monoubiquitination at Lys644. Lymphomas with Lys644 mutants have diminished survival.
The production of type I interferon is regulated by the master transcription factor IRF7. Kim and colleagues show that OASL1 specifically recognizes IRF7 mRNA and inhibits its translation and the production of type I interferon.
CD8+ T cell are primed via recognition of cognate peptides presented by APCs. Krummel and colleagues show that optimal CD8+ T cell differentiation then occurs via T cell–T cell interactions dependent on the integrin LFA-1.
Thymic stromal lymphopoietin promotes type 2 allergic immune responses via the transcription factor STAT5. Ziegler and colleagues show that ablation of STAT5 in DCs prevents type 2 but not type 1 immunity.
IgA is essential in the maintenance of mucosal host defense and intestinal homeostasis. Stockinger and colleagues show that TH17 cells acquire a follicular helper T cell phenotype in Peyer's patches and induce the development of IgA-producing B cells.
The transcriptional repressor Bcl-6 operates in many hematopoietic lineages. Melnick and colleagues show that Bcl-6 with a mutant BTB corepressor interaction domain selectively impairs B cell effector function.
NKp46+ innate lymphoid cells are important for the control of gut microbes, but their development is unclear. Belz and colleagues show that they develop from lymphoid tissue–inducer cells in a Notch- and T-bet-dependent manner.
Retrotransposons are often thought of as 'selfish' genetic elements that replicate themselves without any obvious benefit to the host genome. Saleh and colleagues demonstrate that retrotransposons can be involved in generating silencing RNA species to regulate viral replication.
Antigenic activation induces the generation of effector and memory CD8+ T cells. Goldrath and colleagues profile gene expression at various times after infection to identify transcriptional networks unique to each population.