Please use this identifier to cite or link to this item: 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

Show full item record
Files in This Item:
File Description SizeFormatAccess SettingsVersion 
10_4049_jimmunol_1101854.pdf4.23 MBAdobe PDF

OPEN

NoneView/Download

SCOPUSTM   
Citations

39
checked on Apr 22, 2021

Page view(s)

50
checked on Apr 16, 2021

Google ScholarTM

Check

Altmetric


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.