File Download
  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: The role of regulatory B cells during the progression of human hepatocellular carcinoma

TitleThe role of regulatory B cells during the progression of human hepatocellular carcinoma
Authors
Issue Date2012
PublisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org
Citation
Journal of Immunology, v. 188 meeting abstract suppl., abstract 162.39 How to Cite?
AbstractHong Kong Human regulatory B cells (hBregs) have been shown to play an important role in autoimmune diseases, but their function during human cancer progression remains elusive. In this study, we aim to unveil the underlying mechanism of hBregs regulating human hepatocellular carcinoma (HCC) growth. B cells in HCC liver tumor were examined by immunohistochemistry. We found a tendency that the amount of B cells increased with HCC progression (p=0.001), and it’s in the marginal region of HCC increased (P<0.001) more dramatically. In vitro, human HCC cell line MHCC-97L cells were cocultured with hBregs. hBregs promoted HCC cells proliferation (P=0.011) and migration (p=0.006) and decreased HCC cells apoptosis (p=0.078). HCC cells also promoted hBregs proliferation and migration (p=0.003). hBregs could interact with HCC cells directly through CD40-CD154 signaling. Tail vein injection of hBreg cells into SCID mice increased the size of HCC xenograft tumor (4 weeks, p=0.0221). In vivo imagining showed that hBreg cells could migrate into tumor. Our findings indicate that hBregs could promote HCC progression.
DescriptionOpen Access Journal
Persistent Identifierhttp://hdl.handle.net/10722/160393
ISSN
2014 Impact Factor: 4.922
2014 SCImago Journal Rankings: 3.031

 

DC FieldValueLanguage
dc.contributor.authorShao, Yen_US
dc.contributor.authorLi, Cen_US
dc.contributor.authorMa, YYen_US
dc.contributor.authorLiu, Xen_US
dc.contributor.authorChu, CYen_US
dc.contributor.authorLing, Cen_US
dc.contributor.authorYeung, WHen_US
dc.contributor.authorLee, KWen_US
dc.contributor.authorFan, STen_US
dc.contributor.authorLo, CMen_US
dc.contributor.authorMan, K-
dc.date.accessioned2012-08-16T06:09:36Z-
dc.date.available2012-08-16T06:09:36Z-
dc.date.issued2012en_US
dc.identifier.citationJournal of Immunology, v. 188 meeting abstract suppl., abstract 162.39en_US
dc.identifier.issn0022-1767-
dc.identifier.urihttp://hdl.handle.net/10722/160393-
dc.descriptionOpen Access Journal-
dc.description.abstractHong Kong Human regulatory B cells (hBregs) have been shown to play an important role in autoimmune diseases, but their function during human cancer progression remains elusive. In this study, we aim to unveil the underlying mechanism of hBregs regulating human hepatocellular carcinoma (HCC) growth. B cells in HCC liver tumor were examined by immunohistochemistry. We found a tendency that the amount of B cells increased with HCC progression (p=0.001), and it’s in the marginal region of HCC increased (P<0.001) more dramatically. In vitro, human HCC cell line MHCC-97L cells were cocultured with hBregs. hBregs promoted HCC cells proliferation (P=0.011) and migration (p=0.006) and decreased HCC cells apoptosis (p=0.078). HCC cells also promoted hBregs proliferation and migration (p=0.003). hBregs could interact with HCC cells directly through CD40-CD154 signaling. Tail vein injection of hBreg cells into SCID mice increased the size of HCC xenograft tumor (4 weeks, p=0.0221). In vivo imagining showed that hBreg cells could migrate into tumor. Our findings indicate that hBregs could promote HCC progression.-
dc.languageengen_US
dc.publisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.orgen_US
dc.relation.ispartofJournal of Immunologyen_US
dc.titleThe role of regulatory B cells during the progression of human hepatocellular carcinomaen_US
dc.typeConference_Paperen_US
dc.identifier.emailShao, Y: yshao@hku.hken_US
dc.identifier.emailLi, C: doclicx@hku.hken_US
dc.identifier.emailMa, YY: yyma@hku.hken_US
dc.identifier.emailLiu, X: liuxb301@hku.hken_US
dc.identifier.emailChu, CY: bcccy@HKUSUA.hku.hken_US
dc.identifier.emailLing, C: lingccl@hku.hken_US
dc.identifier.emailYeung, WH: whoy@HKUSUC.hku.hken_US
dc.identifier.emailLee, KW: tkwlee@hkucc.hku.hken_US
dc.identifier.emailFan, ST: stfan@hku.hken_US
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hk-
dc.identifier.emailMan, K: kwanman@hku.hk-
dc.identifier.authorityLee, KW=rp00447en_US
dc.identifier.authorityFan, ST=rp00355en_US
dc.identifier.authorityLo, CM=rp00412en_US
dc.identifier.authorityMan, K=rp00417en_US
dc.description.naturelink_to_OA_fulltext-
dc.identifier.hkuros202992en_US
dc.identifier.volume188en_US
dc.identifier.issuemeeting abstract suppl.-
dc.publisher.placeUnited States-
dc.customcontrol.immutablesml 130320-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats