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Tonsil-derived mesenchymal stromal cells produce CXCR2-binding chemokines and acquire follicular dendritic cell-like phenotypes under TLR3 stimulation

Title
Tonsil-derived mesenchymal stromal cells produce CXCR2-binding chemokines and acquire follicular dendritic cell-like phenotypes under TLR3 stimulation
Authors
Ryu, Jung-HwaPark, MinhwaKim, Bo-KyungRyu, Kyung-HaWoo, So-Youn
Ewha Authors
유경하우소연
SCOPUS Author ID
유경하scopus; 우소연scopus
Issue Date
2015
Journal Title
CYTOKINE
ISSN
1043-4666JCR Link1096-0023JCR Link
Citation
vol. 73, no. 2, pp. 225 - 235
Keywords
Toll-like receptorsTonsil-derived mesenchymal stromal cellsCXCR2CD54B cells
Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
Indexed
SCI; SCIE; SCOPUS WOS
Abstract
We previously isolated mesenchymal stromal cells from human tonsils (T-MSCs) and showed the potential of these cells to differentiate into the mesodermal lineage and acquire a follicular dendritic cell (FDC) phenotype under cytokine stimulation. Because these T-MSCs were originally isolated from inflamed tonsillar tissues, we were curious about their activation status in response to innate immune stimuli, such as Toll-like receptors (TLRs). Therefore, we analyzed the expression profile of TLRs in T-MSCs and stimulated the T-MSCs with TLR agonists. TLR3 stimuli induced C-C chemokine receptor type 6 expression in T-MSCs after 24 h. Furthermore, results from cytokine arrays showed increases in epithelial neutrophil-activating peptide-78/C-X-C motif chemokine (CXCL) 5, granulocyte chemotactic protein-2/CXCL6, growth-related oncogene-alpha/CXCL1, interleukin-8/CXCL8, and interferon gamma-induced protein-10/CXCL10. CD54 expression was also increased after TLR3 stimulation. However, co-culturing T-MSCs with human B cells did not induce B-cell proliferation. This suggests that TLR3 stimulates the differentiation of T-MSCs into FDC-like cells and induces chemokine secretion, possibly by recruiting C-X-C chemokine receptor 2-expressing immune cells. In addition, T-MSCs also appeared to exert immunomodulatory effects by inhibiting B-cell proliferation, possibly by down-regulating CD18. (C) 2015 Elsevier Ltd. All rights reserved.
DOI
10.1016/j.cyto.2015.02.028
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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