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- W1645084103 abstract "Abstract Lymph node stromal cells (LNSCs) closely regulate immunity and self-tolerance, yet key aspects of their biology remain poorly illuminated. Little is known about what factors these cells produce beyond a short list of critical molecules, or how these subsets respond to inflammation. Comparative transcriptomic analyses of steady-state murine LNSC subsets revealed expression of important immune mediators and growth factors. Further, pairwise analyses of ligand and cognate receptor expression by hematopoietic and stromal subsets suggested a complex web of cross-talk. Transcriptional profiling of steady-state LNSC subsets also suggested a readiness of these cells to respond to inflammatory and infectious triggers. Accordingly, fibroblastic reticular cells (FRCs), blood endothelial cells (BECs), and lymphatic endothelial cells (LECs) isolated from inflamed lymph nodes upregulated expression of numerous genes involved in the acute phase response, immune cell recruitment, and the MHC II antigen processing and presentation pathway, among others. Flow cytometric analysis demonstrated elevated levels of surface MHC II on FRCs, BECs, and LECs isolated from skin-draining lymph nodes 18 hours after the onset of inflammation. LNSC subsets from inflamed lymph nodes also produced the antimicrobial molecule lipocalin 2. Together these data offer insight into the transcriptional identities of murine LNSC subsets, while suggesting that they may be active players during ongoing inflammation." @default.
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- W1645084103 date "2012-05-01" @default.
- W1645084103 modified "2023-09-27" @default.
- W1645084103 title "Transcriptional profiling of steady-state and inflamed lymph node stroma reveals potential hematopoietic-stromal cross-talk pathways and suggests an active role for stroma during ongoing immune responses. (176.22)" @default.
- W1645084103 doi "https://doi.org/10.4049/jimmunol.188.supp.176.22" @default.
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