Effects of heat shock protein gp96 on human dendritic cell maturation and CTL expansion

Zhang, Yuxia; Zan, Yanlu; Shan, Ming; Liu, Chang‐Mei; Shi, Ming; Li, Wei; Zhang, Zhixin; Liu, Na; Wang, Fusheng; Zhong, Weidong; Liao, Fulian; Gao, George F.; Tien, Po

doi:10.1016/j.bbrc.2006.03.171

Cited by 26 publications

(23 citation statements)

References 33 publications

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“…13,36,39 Several studies have shown that gp96-associated peptides could anchor antigen on the cell membrane and directly present it to natural killer cells or cd + T cells as superantigen without being dependent on the stimulation of MHC-I molecules. 33,34,40,41 In the present study, tumor rejection assay demonstrated that cross-linking protein vaccine gp96/AFP elicited strong specific antitumor immunity against AFPproducing H22 cells than AFP vaccination alone. Results indicated that AFP immunogenicity could be greatly improved by gp96 and vaccination with gp96 could increase T-cell proliferation responses to AFP.…”

Section: Discussionmentioning

confidence: 83%

Glycoprotein 96 and α-Fetoprotein Cross-Linking Complexes Elicited Specific Antitumor Immunity

Wang

Wang²,

Lin³

et al. 2013

Cancer Biotherapy and Radiopharmaceuticals

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Hepatocellular carcinoma (HCC) is one of the most common malignant gastroenterological cancers over the world. α-fetoprotein (AFP) is an oncofetal protein produced during HCC development that could generate weaker and less reproducible antitumor protection, and it may serve as a target for immunotherapy. Therefore, it is imperative to enhance its immunogenicity and develop therapeutic vaccines to eliminate AFP-expressing tumors. In this study, by way of glutaraldehyde cross-linking, we constructed a potential therapeutic protein vaccine, glycoprotein 96 (gp96)/AFP. Our results demonstrated that AFP and gp96 synergistically exhibited significant increase in AFP-specific CD8⁺ T-cell responses and impressive cytotoxic antitumor effect against AFP-expressing tumors. Priming mice with the reconstructed vaccine, we elicited robust strong protective immunity. Our study suggests that tumor vaccine by cross-linking tumor antigen and gp96 is a promising approach to cancer therapy.

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Section: Discussionmentioning

confidence: 83%

Glycoprotein 96 and α-Fetoprotein Cross-Linking Complexes Elicited Specific Antitumor Immunity

Wang

Wang²,

Lin³

et al. 2013

Cancer Biotherapy and Radiopharmaceuticals

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“…It has been reported that vaccination of mice with heat-stressed autologous apoptotic tumor cells induces strong antitumor immunity compared with non-stressed cells, and heat-stressed apoptotic tumor cells are effective immunogens when loaded onto syngeneic DCs [7]. One mechanism for enhancement of antitumor immunity by heat-stressed apoptotic tumor cells might be through increased surface expression of HSPs because HSPs have adjuvant effects on DC maturation and CTL expansion [13,14]. In this study, we also found that heat-stressed lymphoma cell lines expressed higher levels of HSPs.…”

Section: Discussionmentioning

confidence: 98%

Enhancement of anti-lymphoma immuno-effects mediated by dendritic cells pulsed with heat-stressed and rituximab-coated CD20+ lymphoma cells

Ren

Shi

et al. 2008

Int J Hematol

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Rituximab, a CD20-reactive chimeric monoclonal antibody (mAb), induces apoptosis of lymphoma cells and promotes phagocytosis by dendritic cells and produces a cellular immunoresponse by cross-presentation of tumor antigens to T cells. Heat-stressed tumor cells also stimulate dendritic-cell maturation and induce specific cytotoxic T cells against tumor cells by inducing expression of heat-shock proteins. In this study, we used heat-stressed and rituximab-coated CD20+ lymphoma cells as antigens to load onto immature dendritic cells, and found that rituximab-coated CD20+ Raji cells could promote phagocytosis by dendritic cells, and that rituximab-coated or heat-stressed and then rituximab-coated CD20+ Raji cells resulted in increased dendritic cell maturation. Moreover, only CD20+ Raji cells treated with heat and rituximab effectively enhanced the immunostimulating functions of dendritic cells. Thus, our data indicate that rituximab and heat-shock proteins have synergistic effects, resulting in increased induction of cytotoxic T cells against B-cell lymphoma.

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“…Several genes, ADA, Tnfrs17 and Siva, known to be involved in lymphocyte functioning (Hatzoglou et al, 2000;Mishra et al, 2005;Gudi et al, 2006;Trem et al, 2006), were found to be up-regulated by PE. Gp96, is involved in innate and adaptive immune response (Rivoltinie et al, 2003, Zhang et al, 2006.…”

Section: Discussion and Conlusionsmentioning

confidence: 99%

“…Gp96 is especially involved in the immune response to tumor antigens by chaperoning tumor antigen-derived immunogenic peptides and deliver them to antigen-presenting cells for specific T-lymphocyte stimulation. Gp96 also mediates the maturation of DCs by up-regulating the expression of MHC Class II and co-stimulatory molecules (Rivoltini et al, 2003;Zhang et al, 2006).…”

Section: Gene Expression Profilesmentioning

confidence: 99%

Gene expression changes in the mesenteric lymph nodes of rats after oral peanut extract exposure

Jonge

Pennings

Baken

et al. 2008

Journal of Immunotoxicology

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Effects of heat shock protein gp96 on human dendritic cell maturation and CTL expansion

Cited by 26 publications

References 33 publications

Glycoprotein 96 and α-Fetoprotein Cross-Linking Complexes Elicited Specific Antitumor Immunity

Glycoprotein 96 and α-Fetoprotein Cross-Linking Complexes Elicited Specific Antitumor Immunity

Enhancement of anti-lymphoma immuno-effects mediated by dendritic cells pulsed with heat-stressed and rituximab-coated CD20+ lymphoma cells

Gene expression changes in the mesenteric lymph nodes of rats after oral peanut extract exposure

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