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CD86 Is an Activation Receptor for NK Cell Cytotoxicity against Tumor Cells (CTLA4Ig Activate NK Cell via Ligation of CD86)

CTLA4Ig has been successfully used in the clinic for suppression of T cell activation. However, patients treated with CTLA4Ig experienced reduced incidence of tumors than predicted, but the underlying mechanism remains unknown. In this paper, we showed that brief administration of CTLA4Ig significan... Full description

Journal Title: 2013 Vol.8(12), p.e83913
Main Author: Peng, Yanmeng
Other Authors: Luo, Gaoxing , Zhou, Junyi , Wang, Xiaojuan , Hu, Jie , Cui, Yanyan , Li, Xian C , Tan, Jianglin , Yang, Sisi , Zhan, Rixing , Yang, Junjie , He, Weifeng , Wu, Jun
Format: Electronic Article Electronic Article
Language: English
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ID: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0083913
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recordid: plos10.1371/journal.pone.0083913
title: CD86 Is an Activation Receptor for NK Cell Cytotoxicity against Tumor Cells (CTLA4Ig Activate NK Cell via Ligation of CD86)
format: Article
creator:
  • Peng, Yanmeng
  • Luo, Gaoxing
  • Zhou, Junyi
  • Wang, Xiaojuan
  • Hu, Jie
  • Cui, Yanyan
  • Li, Xian C
  • Tan, Jianglin
  • Yang, Sisi
  • Zhan, Rixing
  • Yang, Junjie
  • He, Weifeng
  • Wu, Jun
subjects:
  • Research Article
ispartof: 2013, Vol.8(12), p.e83913
description: CTLA4Ig has been successfully used in the clinic for suppression of T cell activation. However, patients treated with CTLA4Ig experienced reduced incidence of tumors than predicted, but the underlying mechanism remains unknown. In this paper, we showed that brief administration of CTLA4Ig significantly reduced tumor metastasis and prolonged the survival of host mice bearing B16 melanoma. Depletion of NK cells prior to CTLA4Ig administration eliminated the CTLA4Ig-mediated anti-tumor activity. CTLA4Ig enhanced NK cell cytotoxicity to tumor cells via up-regulation of NK cell effecter molecules CD107a and perforin in vivo . In addition, we demonstrated that, upon activation, NK cells could significantly increase the expression of CD86 both in vitro and in vivo , and ligation of CD86 with CTLA4Ig significantly increased the ability of NK cells to kill tumor cells. Furthermore, a human NK cell line that expressed high level of CD86 was directly activated by CTLA4Ig so that killing of tumor targets was enhanced; this enhanced killing could be inhibited by blocking CD86. Our findings uncover a novel function of CTLA4Ig in tumor immunity and suggest that CD86 on NK cells is an activating receptor and closely involved in the CTLA4Ig-mediated anti-tumor response.
language: eng
source:
identifier: E-ISSN: 1932-6203 ; DOI: 10.1371/journal.pone.0083913
fulltext: fulltext
issn:
  • 1932-6203
  • 19326203
url: Link


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titleCD86 Is an Activation Receptor for NK Cell Cytotoxicity against Tumor Cells (CTLA4Ig Activate NK Cell via Ligation of CD86)
creatorPeng, Yanmeng ; Luo, Gaoxing ; Zhou, Junyi ; Wang, Xiaojuan ; Hu, Jie ; Cui, Yanyan ; Li, Xian C ; Tan, Jianglin ; Yang, Sisi ; Zhan, Rixing ; Yang, Junjie ; He, Weifeng ; Wu, Jun
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descriptionCTLA4Ig has been successfully used in the clinic for suppression of T cell activation. However, patients treated with CTLA4Ig experienced reduced incidence of tumors than predicted, but the underlying mechanism remains unknown. In this paper, we showed that brief administration of CTLA4Ig significantly reduced tumor metastasis and prolonged the survival of host mice bearing B16 melanoma. Depletion of NK cells prior to CTLA4Ig administration eliminated the CTLA4Ig-mediated anti-tumor activity. CTLA4Ig enhanced NK cell cytotoxicity to tumor cells via up-regulation of NK cell effecter molecules CD107a and perforin in vivo . In addition, we demonstrated that, upon activation, NK cells could significantly increase the expression of CD86 both in vitro and in vivo , and ligation of CD86 with CTLA4Ig significantly increased the ability of NK cells to kill tumor cells. Furthermore, a human NK cell line that expressed high level of CD86 was directly activated by CTLA4Ig so that killing of tumor targets was enhanced; this enhanced killing could be inhibited by blocking CD86. Our findings uncover a novel function of CTLA4Ig in tumor immunity and suggest that CD86 on NK cells is an activating receptor and closely involved in the CTLA4Ig-mediated anti-tumor response.
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titleCD86 Is an Activation Receptor for NK Cell Cytotoxicity against Tumor Cells (CTLA4Ig Activate NK Cell via Ligation of CD86)
descriptionCTLA4Ig has been successfully used in the clinic for suppression of T cell activation. However, patients treated with CTLA4Ig experienced reduced incidence of tumors than predicted, but the underlying mechanism remains unknown. In this paper, we showed that brief administration of CTLA4Ig significantly reduced tumor metastasis and prolonged the survival of host mice bearing B16 melanoma. Depletion of NK cells prior to CTLA4Ig administration eliminated the CTLA4Ig-mediated anti-tumor activity. CTLA4Ig enhanced NK cell cytotoxicity to tumor cells via up-regulation of NK cell effecter molecules CD107a and perforin in vivo . In addition, we demonstrated that, upon activation, NK cells could significantly increase the expression of CD86 both in vitro and in vivo , and ligation of CD86 with CTLA4Ig significantly increased the ability of NK cells to kill tumor cells. Furthermore, a human NK cell line that expressed high level of CD86 was directly activated by CTLA4Ig so that killing of tumor targets was enhanced; this enhanced killing could be inhibited by blocking CD86. Our findings uncover a novel function of CTLA4Ig in tumor immunity and suggest that CD86 on NK cells is an activating receptor and closely involved in the CTLA4Ig-mediated anti-tumor response.
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abstractCTLA4Ig has been successfully used in the clinic for suppression of T cell activation. However, patients treated with CTLA4Ig experienced reduced incidence of tumors than predicted, but the underlying mechanism remains unknown. In this paper, we showed that brief administration of CTLA4Ig significantly reduced tumor metastasis and prolonged the survival of host mice bearing B16 melanoma. Depletion of NK cells prior to CTLA4Ig administration eliminated the CTLA4Ig-mediated anti-tumor activity. CTLA4Ig enhanced NK cell cytotoxicity to tumor cells via up-regulation of NK cell effecter molecules CD107a and perforin in vivo . In addition, we demonstrated that, upon activation, NK cells could significantly increase the expression of CD86 both in vitro and in vivo , and ligation of CD86 with CTLA4Ig significantly increased the ability of NK cells to kill tumor cells. Furthermore, a human NK cell line that expressed high level of CD86 was directly activated by CTLA4Ig so that killing of tumor targets was enhanced; this enhanced killing could be inhibited by blocking CD86. Our findings uncover a novel function of CTLA4Ig in tumor immunity and suggest that CD86 on NK cells is an activating receptor and closely involved in the CTLA4Ig-mediated anti-tumor response.
copSan Francisco, USA
pubPublic Library of Science
doi10.1371/journal.pone.0083913
oafree_for_read
date2013-12-11