Adaptive immunity is initiated in T-cell zones of secondary lymphoid organs. These zones are organized in a rigid 3D network of fibroblastic reticular cells (FRCs) that are a rich cytokine source. In response to lymph-borne antigens, draining lymph nodes (LNs) expand several folds in size, but the fate and role of the FRC network during immune response is not fully understood. Here we show that T-cell responses are accompanied by the rapid activation and growth of FRCs, leading to an expanded but similarly organized network of T-zone FRCs that maintains its vital function for lymphocyte trafficking and survival. In addition, new FRC-rich environments were observed in the expanded medullary cords. FRCs are activated within hours after the onset of inflammation in the periphery. Surprisingly, FRC expansion depends mainly on trapping of naïve lymphocytes that is induced by both migratory and resident dendritic cells. Inflammatory signals are not required as homeostatic T-cell proliferation was sufficient to trigger FRC expansion. Activated lymphocytes are also dispensable for this process, but can enhance the later growth phase. Thus, this study documents the surprising plasticity as well as the complex regulation of FRC networks allowing the rapid LN hyperplasia that is critical for mounting efficient adaptive immunity.lymph node swelling | fibroblasts | stromal cells | lymphotoxin | MyD88
tRNAs traffic between the nucleus and the cytoplasm in response to nutrient availability. Using a new assay to track tRNA within cells, we show that tRNA nuclear import is constitutive, whereas tRNA reexport to the cytoplasm is regulated. Msn5 functions only in tRNA re-export, whereas Los1 functions in both the primary and reexport steps.
Highlights d RNA polymerase IV, RDR2, and DCL3 are sufficient for siRNA synthesis in vitro d Nontemplate-strand-induced Pol IV termination triggers RDR2 synthesis of dsRNA d RDR2 adds an untemplated terminal nucleotide to its transcripts' 3 0 ends d DCL3 generates 24-and 23-nt siRNAs; 23-nt siRNAs often have untemplated termini
Fasnacht et al. now show that fibroblasts in secondary lymphoid organs are responsible for the production of Notch ligands regulating the differentiation of immune cells
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