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Article: Increased expression of mGITRL on D2SC/1 cells by particulate β-glucan impairs the suppressive effect of CD4 +CD25 + regulatory T cells and enhances the effector T cell proliferation

TitleIncreased expression of mGITRL on D2SC/1 cells by particulate β-glucan impairs the suppressive effect of CD4 +CD25 + regulatory T cells and enhances the effector T cell proliferation
Authors
Issue Date2011
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ycimm
Citation
Cellular Immunology, 2011, v. 270 n. 2, p. 183-187 How to Cite?
Abstract
β-Glucans have been shown to enhance immune responses for centuries, which contributes to their anti-tumor property. However, their mechanisms of action are still elusive. Dectin-1, the C-type lectin receptor for β-glucan, is expressed abundantly on dendritic cells (DCs). Activation of DCs via Dectin-1 can lead to the maturation of DC, inducing both innate and adaptive immune responses against tumor development and microbial infection. In this study, we found that particulate yeast-derived β-glucans could induce the maturation of murine dendritic cell line D2SC/1 cells and increase the expression of mGITRL on D2SC/1 cells via Dectin-1/Syk pathway in a dose dependent manner. Furthermore, we demonstrated that the increased mGITRL on D2SC/1 cells could impair the suppressive activity of CD4 +CD25 + regulatory T cells (Tregs) and enhance the proliferation of CD4 +CD25 - effector T cells (Teffs). These findings suggest that particulate β-glucan can be used as immunomodulator to stimulate potent T cell-mediated adaptive immunity while down-regulate immune suppressive activity, leading to a more efficient defense mechanism against tumor development or infectious diseases. © 2011 Elsevier Inc.
Persistent Identifierhttp://hdl.handle.net/10722/148645
ISSN
2013 Impact Factor: 1.874
ISI Accession Number ID
Funding AgencyGrant Number
National Natural Science Foundation of China81072453
30871193
30972748
30910103087
Natural Science Foundation of Jiangsu ProvinceBK2004405
Natural Science Foundation of Jiangsu Province Educational Commission08KJB320002
Health Department Foundation of Jiangsu ProvinceH200952
Jiangsu University
SCI-Tech Innovation Team of Jiangsu University
Funding Information:

This study was supported by National Natural Science Foundation of China (Grant No. 81072453, 30871193, 30972748, 30910103087), Natural Science Foundation of Jiangsu Province (Grant No. BK2004405), Natural Science Foundation of Jiangsu Province Educational Commission (Grant No. 08KJB320002), Health Department Foundation of Jiangsu Province (Grant No.H200952), Jiangsu Province Qing Lan Project, and Top Talent Program of Jiangsu University and SCI-Tech Innovation Team of Jiangsu University.

References

 

Author Affiliations
  1. Jiangsu University
  2. The University of Hong Kong
  3. null
DC FieldValueLanguage
dc.contributor.authorTian, Jen_US
dc.contributor.authorMa, Jen_US
dc.contributor.authorWang, Sen_US
dc.contributor.authorYan, Jen_US
dc.contributor.authorChen, Jen_US
dc.contributor.authorTong, Jen_US
dc.contributor.authorWu, Cen_US
dc.contributor.authorLiu, Yen_US
dc.contributor.authorMa, Ben_US
dc.contributor.authorMao, Cen_US
dc.contributor.authorJiao, Zen_US
dc.contributor.authorShao, Qen_US
dc.contributor.authorLu, Len_US
dc.contributor.authorXu, Hen_US
dc.date.accessioned2012-05-29T06:14:20Z-
dc.date.available2012-05-29T06:14:20Z-
dc.date.issued2011en_US
dc.identifier.citationCellular Immunology, 2011, v. 270 n. 2, p. 183-187en_US
dc.identifier.issn0008-8749en_US
dc.identifier.urihttp://hdl.handle.net/10722/148645-
dc.description.abstractβ-Glucans have been shown to enhance immune responses for centuries, which contributes to their anti-tumor property. However, their mechanisms of action are still elusive. Dectin-1, the C-type lectin receptor for β-glucan, is expressed abundantly on dendritic cells (DCs). Activation of DCs via Dectin-1 can lead to the maturation of DC, inducing both innate and adaptive immune responses against tumor development and microbial infection. In this study, we found that particulate yeast-derived β-glucans could induce the maturation of murine dendritic cell line D2SC/1 cells and increase the expression of mGITRL on D2SC/1 cells via Dectin-1/Syk pathway in a dose dependent manner. Furthermore, we demonstrated that the increased mGITRL on D2SC/1 cells could impair the suppressive activity of CD4 +CD25 + regulatory T cells (Tregs) and enhance the proliferation of CD4 +CD25 - effector T cells (Teffs). These findings suggest that particulate β-glucan can be used as immunomodulator to stimulate potent T cell-mediated adaptive immunity while down-regulate immune suppressive activity, leading to a more efficient defense mechanism against tumor development or infectious diseases. © 2011 Elsevier Inc.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ycimmen_US
dc.relation.ispartofCellular Immunologyen_US
dc.subject.meshAdaptive Immunity - Drug Effectsen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshCell Lineen_US
dc.subject.meshCell Proliferation - Drug Effectsen_US
dc.subject.meshDendritic Cells - Drug Effects - Immunologyen_US
dc.subject.meshDose-Response Relationship, Immunologicen_US
dc.subject.meshGene Expression - Drug Effectsen_US
dc.subject.meshImmunologic Factors - Administration & Dosage - Pharmacologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred Balb Cen_US
dc.subject.meshRna, Messenger - Geneticsen_US
dc.subject.meshT-Lymphocyte Subsets - Cytology - Immunologyen_US
dc.subject.meshT-Lymphocytes, Regulatory - Immunologyen_US
dc.subject.meshTumor Necrosis Factors - Geneticsen_US
dc.subject.meshBeta-Glucans - Administration & Dosage - Immunology - Pharmacologyen_US
dc.titleIncreased expression of mGITRL on D2SC/1 cells by particulate β-glucan impairs the suppressive effect of CD4 +CD25 + regulatory T cells and enhances the effector T cell proliferationen_US
dc.typeArticleen_US
dc.identifier.emailLu, L:liweilu@hkucc.hku.hken_US
dc.identifier.authorityLu, L=rp00477en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.cellimm.2011.05.003en_US
dc.identifier.pmid21636079en_US
dc.identifier.scopuseid_2-s2.0-80051667327en_US
dc.identifier.hkuros208185-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80051667327&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume270en_US
dc.identifier.issue2en_US
dc.identifier.spage183en_US
dc.identifier.epage187en_US
dc.identifier.isiWOS:000294319300010-
dc.publisher.placeUnited Statesen_US
dc.identifier.citeulike9318091-

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