Mice were challenged with C1498 and then treated with cytarabine.
The publication costs of this article were defrayed in part by page charge payment. Statistical analysis compared unvaccinated and vaccinated with α-GalCer–pulsed irradiated leukemia cell groups.
Please enable it to take advantage of the complete set of features! FSC-A, forward scatter area; MFI, mean fluorescent intensity; SSC, side scatter. Int J Cancer 2011;129(6):1373-1381.
eCollection 2019. J. Virol. Race and ethnicity in decisions about unrelated hematopoietic stem cell donation.
(F-G) The splenic langerin+CD8α+ DC population in lang-EGFP mice was analyzed 24 hours after vaccination. Postremission therapies with reduced toxicities are urgently needed. 2020 May 11;39(1):85. doi: 10.1186/s13046-020-01580-4. Analysis was performed with Prism 5.0 software (GraphPad Software, Inc.); P values <.05 were considered significant. In comparison with vaccination with defined antigens, an α-GalCer–loaded autologous whole cell vaccine for acute leukemia has the advantages of stimulating both innate and daptive immunity and covering a broad range of leukemia-associated antigens without being limited by HLA phenotype.
Nat. (E) The proportion of MDSCs within live splenocytes. These permits may be required for shipping this product: ISO 17025
Are you sure? Use of allogeneic hematopoietic stem-cell transplantation based on minimal residual disease response improves outcomes for children with relapsed acute lymphoblastic leukemia in the intermediate-risk group. analyzed and interpreted the data and wrote the manuscript; J.D.G. See Hartley and Rowe (1975.
(B) Percentage of Tregs in the spleens and livers of naïve and leukemia-challenged mice.
Utilizing the adjuvant properties of CD1d-dependent NK T cells in T cell-mediated immunotherapy. (D) Flow cytometric identification of splenic CD11b+Ly6G+ MDSCs.
(F) lang-EGFPDTR mice were prophylactically vaccinated, and 1 group was administered DT. Therefore, detailed mechanisms of refractoriness, including leukemia-initiating cell (LIC) biology, should be elucidated to treat AML.
These findings have implications for the design of clinical trials that test immunotherapies for acute leukemias. Clin Cancer Res. Chemotherapy restores the T-cell compartment in leukemic mice. Bars and error bars in the figures depict the mean and standard deviation of the mean. ***Please note that cell lines are not for sale and unavailable for purchase from Covance. Regulatory T cell lineage specification by the forkhead transcription factor foxp3. Hum Vaccin. The glycolipid α-GalCer acts as an adjuvant via a third-party mechanism by binding to CD1d on DCs and recruiting NKT cells to create a stimulatory environment that leads to enhanced peptide-specific responses by conventional CD4+ and CD8+ effector T cells.23,47,63 Although CD1d is weakly expressed on C1498 cells and has been identified in other acute leukemic cell lines, including AML-ETO9a,23 EL4, and WEHI-3B (L.R.A, unpublished data, June 14, 2014), we have previously demonstrated that a CD1d-negative α-GalCer–pulsed glioma vaccine can provide protection against glioma challenge.25 We have also shown that CD1d-deficient DCs can transfer α-GalCer to host resident CD1d-expressing antigen-presenting cells in vivo to induce potent invariant NKT-cell activation, which likely reflects transfer of α-GalCer embedded within membranes of the injected cells.46 It is therefore not necessary for NKT cells to interact directly via CD1d on the cells of the vaccine to provide adjuvant activity.
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Oncogene.
doi: 10.1038/nrc2091. By using the aggressive acute leukemia cell line C1498,62 we show that a simple vaccine comprising whole irradiated leukemia cells pulsed with the glycolipid adjuvant α-GalCer protected against the development of leukemia in vivo.
(C-E) Symbols represent treatments: unvaccinated (●), nonleukemic and nonvaccinated (◆), vaccinated with α-GalCer–pulsed irradiated leukemia cells (▪), vaccinated with unpulsed irradiated leukemia cells (□), vaccinated with free α-GalCer (△), depletion of CD4+ cells (▲), and depletion of CD8+ cells (▼). However, given that some antitumor activity was seen in the absence of CD8+ T cells, other CD4+ T-cell functions must be involved, perhaps as effectors in their own right,66 or through interactions with other MHC class II–expressing cells. Interestingly, leukemia challenge was associated with an increase in the percentage of CD8+ T cells expressing the T-cell exhaustion marker programmed-death 1 (PD-1) in the BM, which was unchanged following cytarabine treatment alone. Olme CH, Brown N, Finnon R, Bouffler SD, Badie C. Mutat Res. lang-EGFP hosts were used to identify langerin+CD8α+ DCs by flow cytometry. Clipboard, Search History, and several other advanced features are temporarily unavailable.
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