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https://doi.org/10.4049/jimmunol.1101854
Title: | Expansion of cortical and medullary sinuses restrains lymph node hypertrophy during prolonged inflammation | Authors: | Tan K.W. Yeo K.P. Wong F.H.S. Lim H.Y. Khoo K.L. Abastado J.-P. Angeli V. |
Keywords: | vasculotropin A vasculotropin C animal cell animal tissue article cell migration controlled study cortical sinus dendritic cell experimental model female fibroblast immunocompetent cell inflammation lymph node lymph node hypertrophy lymphadenopathy lymphangiogenesis lymphocyte medullary sinus molecular interaction mouse nonhuman plasticity priority journal protein expression protein localization reticulum cell steady state stroma cell Adoptive Transfer Animals Antibodies, Neutralizing Cell Communication Cell Movement Cell Proliferation Endothelial Cells Female Hypertrophy Inflammation Injections, Intraperitoneal Lymph Nodes Lymphangiogenesis Lymphocytes Mice Mice, Inbred C57BL Mice, Knockout Stromal Cells Vascular Endothelial Growth Factor A |
Issue Date: | 2012 | Citation: | Tan K.W., Yeo K.P., Wong F.H.S., Lim H.Y., Khoo K.L., Abastado J.-P., Angeli V. (2012). Expansion of cortical and medullary sinuses restrains lymph node hypertrophy during prolonged inflammation. Journal of Immunology 188 (8) : 4065-4080. ScholarBank@NUS Repository. https://doi.org/10.4049/jimmunol.1101854 | Abstract: | During inflammation, accumulation of immune cells in activated lymph nodes (LNs), coupled with a transient shutdown in lymphocyte exit, results in dramatic cellular expansion. Counter-regulatory measures to restrain LN expansion must exist and may include re-establishment of lymphocyte egress to steady-state levels. Indeed, we show in a murine model that egress of lymphocytes from LNs was returned to steady-state levels during prolonged inflammation following initial retention. This restoration in lymphocyte egress was supported by a preferential expansion of cortical and medullary sinuses during late inflammation. Cortical and medullary sinus remodeling during late inflammation was dependent on temporal and spatial changes in vascular endothelial growth factor-A distribution. Specifically, its expression was restricted to the subcapsular space of the LN during early inflammation, whereas its expression was concentrated in the paracortical and medullary regions of the LN at later stages. We next showed that this process was mostly driven by the synergistic cross-talk between fibroblastic reticular cells and interstitial flow. Our data shed new light on the biological significance of LN lymphangiogenesis during prolonged inflammation and further underscore the collaborative roles of stromal cells, immune cells, and interstitial flow in modulating LN plasticity and function. © 2012 by The American Association of Immunologists, Inc. | Source Title: | Journal of Immunology | URI: | https://scholarbank.nus.edu.sg/handle/10635/175335 | ISSN: | 0022-1767 | DOI: | 10.4049/jimmunol.1101854 |
Appears in Collections: | Staff Publications Elements |
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