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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
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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
 
AuthorsTian, J1
Ma, J1
Wang, S1
Yan, J3
Chen, J1
Tong, J1
Wu, C1
Liu, Y1
Ma, B1
Mao, C1
Jiao, Z1
Shao, Q1
Lu, L2
Xu, H1
 
Issue Date2011
 
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ycimm
 
CitationCellular Immunology, 2011, v. 270 n. 2, p. 183-187 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.cellimm.2011.05.003
 
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.
 
ISSN0008-8749
2013 Impact Factor: 1.874
 
DOIhttp://dx.doi.org/10.1016/j.cellimm.2011.05.003
 
ISI Accession Number IDWOS:000294319300010
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.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorTian, J
 
dc.contributor.authorMa, J
 
dc.contributor.authorWang, S
 
dc.contributor.authorYan, J
 
dc.contributor.authorChen, J
 
dc.contributor.authorTong, J
 
dc.contributor.authorWu, C
 
dc.contributor.authorLiu, Y
 
dc.contributor.authorMa, B
 
dc.contributor.authorMao, C
 
dc.contributor.authorJiao, Z
 
dc.contributor.authorShao, Q
 
dc.contributor.authorLu, L
 
dc.contributor.authorXu, H
 
dc.date.accessioned2012-05-29T06:14:20Z
 
dc.date.available2012-05-29T06:14:20Z
 
dc.date.issued2011
 
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.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationCellular Immunology, 2011, v. 270 n. 2, p. 183-187 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.cellimm.2011.05.003
 
dc.identifier.citeulike9318091
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.cellimm.2011.05.003
 
dc.identifier.epage187
 
dc.identifier.hkuros208185
 
dc.identifier.isiWOS:000294319300010
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.

 
dc.identifier.issn0008-8749
2013 Impact Factor: 1.874
 
dc.identifier.issue2
 
dc.identifier.pmid21636079
 
dc.identifier.scopuseid_2-s2.0-80051667327
 
dc.identifier.spage183
 
dc.identifier.urihttp://hdl.handle.net/10722/148645
 
dc.identifier.volume270
 
dc.languageeng
 
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/ycimm
 
dc.publisher.placeUnited States
 
dc.relation.ispartofCellular Immunology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshAdaptive Immunity - Drug Effects
 
dc.subject.meshAnimals
 
dc.subject.meshBase Sequence
 
dc.subject.meshCell Line
 
dc.subject.meshCell Proliferation - Drug Effects
 
dc.subject.meshDendritic Cells - Drug Effects - Immunology
 
dc.subject.meshDose-Response Relationship, Immunologic
 
dc.subject.meshGene Expression - Drug Effects
 
dc.subject.meshImmunologic Factors - Administration & Dosage - Pharmacology
 
dc.subject.meshMale
 
dc.subject.meshMice
 
dc.subject.meshMice, Inbred Balb C
 
dc.subject.meshRna, Messenger - Genetics
 
dc.subject.meshT-Lymphocyte Subsets - Cytology - Immunology
 
dc.subject.meshT-Lymphocytes, Regulatory - Immunology
 
dc.subject.meshTumor Necrosis Factors - Genetics
 
dc.subject.meshBeta-Glucans - Administration & Dosage - Immunology - Pharmacology
 
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 proliferation
 
dc.typeArticle
 
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Author Affiliations
  1. Jiangsu University
  2. The University of Hong Kong
  3. null