Combined encapsulation of a tumor antigen and immune cells using a self-assembling immunostimulatory DNA hydrogel to enhance antigen-specific tumor immunity

2018 ◽  
Vol 288 ◽  
pp. 189-198 ◽  
Author(s):  
Yuka Umeki ◽  
Masaaki Saito ◽  
Kosuke Kusamori ◽  
Mari Tsujimura ◽  
Moeka Nishimura ◽  
...  
Keyword(s):  
Tumor Immunity ◽  
Immune Cells ◽  
Tumor Antigen ◽  
Self Assembling ◽  
Specific Tumor ◽  
Dna Hydrogel ◽  
Immunostimulatory Dna

Self-assembling DNA hydrogel-based delivery of immunoinhibitory nucleic acids to immune cells

2016 ◽  
Vol 12 (1) ◽  
pp. 123-130 ◽  
Author(s):  
Yu Nishida ◽  
Shozo Ohtsuki ◽  
Yuki Araie ◽  
Yuka Umeki ◽  
Masayuki Endo ◽  
...  
Keyword(s):  
Nucleic Acids ◽  
Immune Cells ◽  
Self Assembling ◽  
Dna Hydrogel

scholarly journals Estrogen/ER in anti-tumor immunity regulation to tumor cell and tumor microenvironment

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Tiecheng Wang ◽  
Jiakang Jin ◽  
Chao Qian ◽  
Jianan Lou ◽  
Jinti Lin ◽  
...  
Keyword(s):  
Tumor Microenvironment ◽  
Cancer Immunotherapy ◽  
Tumor Immunity ◽  
Immune Cells ◽  
Target Genes ◽  
Target Therapy ◽  
Treatment Strategies ◽  
Signal Transduction Pathway ◽  
Pathway Activation ◽  
Immune System Regulation

AbstractAs the essential sexual hormone, estrogen and its receptor has been proved to participate in the regulation of autoimmunity diseases and anti-tumor immunity. The adjustment of tumor immunity is related to the interaction between cancer cells, immune cells and tumor microenvironment, all of which is considered as the potential target in estrogen-induced immune system regulation. However, the specific mechanism of estrogen-induced immunity is poorly understood. Typically, estrogen causes the nuclear localization of estrogen/estrogen receptor complex and alternates the transcription pattern of target genes, leading to the reprogramming of tumor cells and differentiation of immune cells. However, the estrogen-induced non-canonical signal pathway activation is also crucial to the rapid function of estrogen, such as NF-κB, MAPK-ERK, and β-catenin pathway activation, which has not been totally illuminated. So, the investigation of estrogen modulatory mechanisms in these two manners is vital for the tumor immunity and can provide the potential for endocrine hormone targeted cancer immunotherapy. Here, this review summarized the estrogen-induced canonical and non-canonical signal transduction pathway and aimed to focus on the relationship among estrogen and cancer immunity as well as immune-related tumor microenvironment regulation. Results from these preclinical researches elucidated that the estrogen-target therapy has the application prospect of cancer immunotherapy, which requires the further translational research of these treatment strategies.

scholarly journals Influence of organ site and tumor cell type on MUC1-specific tumor immunity

2001 ◽  
Vol 13 (2) ◽  
pp. 233-240 ◽  
Author(s):  
Keita Morikane ◽  
Richard M. Tempero ◽  
Connie L. Sivinski ◽  
Shimichi Kitajima ◽  
Sandra J. Gendler ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Tumor Immunity ◽  
Cell Type ◽  
Specific Tumor ◽  
Organ Site

scholarly journals The Role of HLA-G in Tumor Escape: Manipulating the Phenotype and Function of Immune Cells

2020 ◽  
Vol 10 ◽  
Author(s):  
Lu Liu ◽  
Lijun Wang ◽  
Lihong Zhao ◽  
Chen He ◽  
Ganlu Wang
Keyword(s):  
T Cells ◽  
Tumor Immunity ◽  
Immune Cells ◽  
Human Leukocyte ◽  
Therapeutic Benefit ◽  
Tumor Escape ◽  
Class I Mhc ◽  
Mhc I ◽  
Suppressive Phenotype ◽  
And Function

Human leukocyte antigen-G (HLA-G) is a non-classical major histocompatibility complex class I (MHC I) molecule, and under physiological conditions, its expression is strictly restricted to the maternal–fetal interface and immune-privileged organs where HLA-G is expected to contribute to establishment and maintenance of immune tolerance. However, the expression of HLA-G has been found in various types of tumors, and the level of its expression frequently correlates with high-grade histology and poor prognosis, raising the possibility that it may play a negative role in tumor immunity. ILT2 and ILT4, present on a broad of immune cells, have been identified as the main receptors engaging HLA-G, and their interactions have been found to allow the conversion of effectors like NK cells and T cells to anergic or unresponsive state, activated DCs to tolerogenic state, and to drive the differentiation of T cells toward suppressive phenotype. Therefore, tumors can employ HLA-G to modulate the phenotype and function of immune cells, allowing them to escape immune attack. In this review, we discuss the mechanism underlying HLA-G expression and function, its role played in each step of the tumor-immunity cycle, as well as the potential to target it for therapeutic benefit.

scholarly journals Development of RNA/DNA Hydrogel Targeting Toll-Like Receptor 7/8 for Sustained RNA Release and Potent Immune Activation

Molecules ◽  
2020 ◽  
Vol 25 (3) ◽  
pp. 728 ◽  
Author(s):  
Fusae Komura ◽  
Kana Okuzumi ◽  
Yuki Takahashi ◽  
Yoshinobu Takakura ◽  
Makiya Nishikawa
Keyword(s):  
Immune Cells ◽  
Dna Nanotechnology ◽  
Dna Assembly ◽  
Toll Like Receptor ◽  
Immunostimulatory Activity ◽  
Dna Nanostructure ◽  
High Level ◽  
Factor Α ◽  
Dna Hydrogel ◽  
Necrosis Factor

Guanosine- and uridine-rich single-stranded RNA (GU-rich RNA) is an agonist of Toll-like receptor (TLR) 7 and TLR8 and induces strong immune responses. A nanostructured GU-rich RNA/DNA assembly prepared using DNA nanotechnology can be used as an adjuvant capable of improving the biological stability of RNA and promoting efficient RNA delivery to target immune cells. To achieve a sustained supply of GU-rich RNA to immune cells, we developed a GU-rich RNA/DNA hydrogel (RDgel) using nanostructured GU-rich RNA/DNA assembly, from which GU-rich RNA can be released in a sustained manner. A hexapod-like GU-rich RNA/DNA nanostructure, or hexapodRD6, was designed using a 20-mer phosphorothioate-stabilized GU-rich RNA and six phosphodiester DNAs. Two sets of hexapodRD6 were mixed to obtain RDgel. Under serum-containing conditions, GU-rich RNA was gradually released from the RDgel. Fluorescently labeled GU-rich RNA was efficiently taken up by DC2.4 murine dendritic cells and induced a high level of tumor necrosis factor-α release from these cells when it was incorporated into RDgel. These results indicate that the RDgel constructed using DNA nanotechnology can be a useful adjuvant in cancer therapy with sustained RNA release and high immunostimulatory activity.

Effect of immunomodulators on specific tumor immunity induced by liposome-encapsulated tumor-associated antigens

1994 ◽  
Vol 56 (5) ◽  
pp. 721-726 ◽  
Author(s):  
Joep J. Bergers ◽  
Willem Den Otter ◽  
Hub F. J. Dullens ◽  
Jan Willem De Groot ◽  
Peter A. Steerenberg ◽  
...  
Keyword(s):  
Tumor Immunity ◽  
Tumor Associated Antigens ◽  
Specific Tumor

A peptide from the known HLA class I restricted melanoma-specific tumor antigen GP100 is presented by HLA-DR in the melanoma cell line FM3

1996 ◽  
Vol 47 (1-2) ◽  
pp. 22
Author(s):  
Thomas Halder ◽  
Graham Pawelec ◽  
Alexei F. Kirkin ◽  
Jesper Zeuthen ◽  
Helmut E. Meyer ◽  
...  
Keyword(s):  
Cell Line ◽  
Melanoma Cell ◽  
Tumor Antigen ◽  
Melanoma Cell Line ◽  
Hla Class I ◽  
Class I ◽  
Hla Dr ◽  
Specific Tumor

scholarly journals Pro-autoimmune allele of tyrosine phosphatase, PTPN22, enhances tumor immunity

2021 ◽  
Author(s):  
Robin C Orozco ◽  
Kristi Marquardt ◽  
Kerri Mowen ◽  
Linda A Sherman
Keyword(s):  
Tumor Immunity ◽  
Immune Cells ◽  
Tumor Response ◽  
Tyrosine Phosphatase ◽  
Cd8 T Cell ◽  
North American Population ◽  
American Population ◽  
Adaptive Immune ◽  
The North ◽  
Adaptive Immune Cells

The 1858C>T allele of the tyrosine phosphatase PTPN22 (causing amino acid substitution R620W in encoded protein Lyp) is present in 5-10% of the North American population and is strongly associated with numerous autoimmune diseases. Although much research has been done to define how this allele potentiates autoimmunity, the influence PTPN22 and its pro-autoimmune allele has in tumor immunity is poorly defined. To interrogate the role this allele may have in the anti-tumor immune response, we used CRISPR/Cas9 to generate mice in which the ortholog of Lyp, PEP, is mutated at position 619 to produce the relevant pro-autoimmune mutation (R619W). Results of this study show that mice homozygous for this alteration (PEP-619WW) resist tumor growth as compared with wildtype mice. Consistent with these results, tumors from PEP-619WW mice have more CD45 infiltrates containing more activated CD8 T cell and CD4 T cells. Additionally, there are more cDC1 cells and less MDSCs in tumors from PEP-619WW mice. Interestingly, the tumor infiltrating PEP-619WW cDC1s have decreased PD-L1 expression compared to cDC1s from PEP-WT mice. Taken together, our data show that the pro-autoimmune allele of Ptpn22 drives a strong anti-tumor response in innate and adaptive immune cells resulting in superior control of tumors.

scholarly journals The Contradictory Role of Interleukin-33 in Immune Cells and Tumor Immunity

2020 ◽  
Vol Volume 12 ◽  
pp. 7527-7537
Author(s):  
Xujun Zhang ◽  
Wenbiao Chen ◽  
Ping Zeng ◽  
Jia Xu ◽  
Hongyan Diao
Keyword(s):  
Tumor Immunity ◽  
Immune Cells ◽  
Interleukin 33

IL-6/STAT3 signaling impaired induction of cancer-antigen specific T cells via down-regulation of dendritic cells in tumor microenvironment.

2015 ◽  
Vol 33 (3_suppl) ◽  
pp. 590-590 ◽  
Author(s):  
Yosuke Ohno ◽  
Hidemitsu Kitamura ◽  
Junya Ohtake ◽  
Shun Kaneumi ◽  
Kentaro Sumida ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
T Cell ◽  
Tumor Immunity ◽  
Immune Cells ◽  
Surface Expression ◽  
Colorectal Cancers ◽  
Expression Levels ◽  
Stat3 Signaling ◽  
Hla Dr

590 Background: Immunosuppression in tumor microenvironments is a critical issue for cancer immunotherapy. Recently, the effectiveness of immuno-check point therapy has been reported on various types of solid tumors. But, the effectiveness in colorectal cancer was poor compared to other cancers, such as melanoma and renal cell carcinoma. Correct regulation of dendritic cell (DC) function in tumors is important for inducing anti-tumor immunity. We have been demonstrated that IL-6 inhibits antigen presentation by DCs through STAT3 activation in tumor-bearing mice. In this study, we focused on the role of the IL-6/STAT3 signaling cascade in human DCs. Methods: Both IL-6 and pSTAT3 expressions in tumor sites of colorectal cancers was verified by immunohistostaining. CD11b+CD11c+DCs in cancer tissues and PBMCs were isolated by fluorescence-activated cell sorting system and investigated about the surface molecules such as HLA-DR, T cell stimulating ability, and effector gene expression levels. Moreover, we investigated influence of IL-6/STAT3 signaling in human DCs in vitro. Results: The results of IHC revealed that IL-6 was preferentially produced by cancer-associated fibroblasts and immune cells in the tissues of colorectal cancers. In addition, it was confirmed that STAT3 was activated in tumor-infiltrating immune cells. Tumor infiltrating CD11b+CD11c+ DCs highly induced IL-6 gene, down-regulated surface expression of HLA-DR, and attenuated T cell stimulating ability. In vitro experiments showed that IL-6-mediated STAT3 activation reduced surface expression of HLA-DR. COX2, cathepsin L (CTSL), and arginase activity were are involved in the IL-6-mediated down-regulation of surface expression levels of HLA-DR expression levels on DCs. Gene expressions of CTSL, ARG1 as well as IL6 in tumor infiltrating CD11b+CD11c+DCs were much higher than those of PBMCs. Conclusions: IL-6-mediated STAT3 activation inhibits functional maturation of DCs, causing suppression of anti-tumor immunity in colorectal cancer. Therefore, inhibition of the IL-6/STAT3 signaling pathway could be a promising strategy for improving immunotherapies for colorectal cancer patients.

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