Relevant bibliographies by topics / Immunology; Tumour cells / Journal articles
To see the other types of publications on this topic, follow the link: Immunology; Tumour cells.

Journal articles on the topic 'Immunology; Tumour cells'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 February 2022

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Immunology; Tumour cells.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Alotaibi, Faizah, Mark Vincent, Weiping Min, and James Koropatnick. "498 Downregulation of CD5 in CD8+ T tumour-infiltrating lymphocytes associates with increased level of activation and exhaustion." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (November 2020): A533. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0498.

Full text
Abstract:
BackgroundCD5, a member of the scavenger receptor cysteine-rich superfamily, is a marker for T cells and a subset of B cells (B1a). CD5 associates with T-cell and B-cell receptors and impair TCR signaling1 2 and increased CD5 is an indication of B cell activation. Furthermore, CD5 levels on CD8+ T cell splenocytes were significantly increased after TCR/CD3 stimulation using ex vivo treatment with anti-CD3/anti-CD28 MAbs compared to non-stimulated CD8+ T splenocytes.3 Previous studies have shown a correlation between CD5 and anti-tumour immunity where CD5 knockout mice inoculated with B16F10 melanoma cells had delayed tumour growth compared to wild type mice.4 In tumour-infiltrating lymphocytes (TILs) isolated from lung cancer patients, CD5 levels were negatively correlated with anti-tumour activity and tumour-mediated activation-induced T cell death,5 suggesting that CD5 could impair activation of anti-tumour T cells. However, the correlation between CD5 level expression and T cell activation and exhaustion in the tumour microenvironment and in peripheral organs is ill-defined and requires further investigation.MethodsWe determined CD5 levels in T cell subsets in different organs in mice bearing syngeneic 4T1 breast tumour homografts and assessed the relationship between CD5 and increased CD69 and PD-1 (markers of T cell activation and exhaustion) by flow cytometry.ResultsWe report that T cell CD5 levels were higher in CD4+ T cells than in CD8+ T cells in 4T1 tumour-bearing mice, and that high CD5 levels on CD4+ T cells were maintained in peripheral organs (spleen and lymph nodes). However, both CD4+ and CD8+ T cells recruited to tumours had reduced CD5 compared to CD4+ and CD8+ T cells in peripheral organs. In addition, CD5highCD4+ T cells and CD5highCD8+ T cells from peripheral organs exhibited higher levels of activation and associated exhaustion compared to CD5lowCD4+ T cell and CD5lowCD8+ T cell from the same organs. Interestingly, CD8+ T cells among TILs and downregulated CD5 were activated to a higher level, with concomitantly increased exhaustion markers, than CD8+CD5+ TILs.ConclusionsThus, differential CD5 levels among T cells in tumours and lymphoid organs can be associated with different levels of T cell activation and exhaustion, suggesting that CD5 may be a therapeutic target for immunotherapeutic activation in cancer therapy.AcknowledgementsThe author thanks Rene Figueredo and Ronak Zareardalan for their assistance in animal workEthics ApprovalThis study was approved by the Animal Use Subcommittee of the University of Western OntarioReferencesAzzam HS, et al., Fine tuning of TCR signaling by CD5. The Journal of Immunology 2001. 166(9): p. 5464–5472.Voisinne GA, Gonzalez de Peredo and Roncagalli R. CD5, an undercover regulator of TCR signaling. Frontiers in Immunology 2018;9:p. 2900.Alotaibi, F., et al., CD5 blockade enhances ex vivo CD8+ T cell activation and tumour cell cytotoxicity. European journal of immunology 2020;50(5): p. 695–704.Tabbekh, M., et al., Rescue of tumor-infiltrating lymphocytes from activation-induced cell death enhances the antitumor CTL response in CD5-deficient mice. The Journal of Immunology, 2011. 187(1): p. 102–109.Dorothée, G., et al., In situ sensory adaptation of tumor-infiltrating T lymphocytes to peptide-MHC levels elicits strong antitumor reactivity. The Journal of Immunology 2005;174(11): p. 6888–6897.
APA, Harvard, Vancouver, ISO, and other styles
2

Ahmad, Sharon. "Tumour cells tout trogocytosis." Nature Reviews Immunology 7, no. 4 (April 2007): 250–51. http://dx.doi.org/10.1038/nri2068.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Cerundolo, Vincenzo. "Tumour immunology: T cells work together to fight cancer." Current Biology 9, no. 18 (September 1999): R695—R697. http://dx.doi.org/10.1016/s0960-9822(99)80442-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Eyileten, Ceren, Kinga Majchrzak, Zofia Pilch, Katarzyna Tonecka, Joanna Mucha, Bartlomiej Taciak, Katarzyna Ulewicz, et al. "Immune Cells in Cancer Therapy and Drug Delivery." Mediators of Inflammation 2016 (2016): 1–13. http://dx.doi.org/10.1155/2016/5230219.

Full text
Abstract:
Recent studies indicate the critical role of tumour associated macrophages, tumour associated neutrophils, dendritic cells, T lymphocytes, and natural killer cells in tumourigenesis. These cells can have a significant impact on the tumour microenvironment via their production of cytokines and chemokines. Additionally, products secreted from all these cells have defined specific roles in regulating tumour cell proliferation, angiogenesis, and metastasis. They act in a protumour capacityin vivoas evidenced by the recent studies indicating that macrophages, T cells, and neutrophils may be manipulated to exhibit cytotoxic activity against tumours. Therefore therapy targeting these cells may be promising, or they may constitute drug or anticancer particles delivery systems to the tumours. Herein, we discussed all these possibilities that may be used in cancer treatment.
APA, Harvard, Vancouver, ISO, and other styles
5

Real, Carla, Francisco Caiado, Catia Igreja, Ana P. Elias, Cristina Borges, Antonio Duarte, and Sergio Dias. "Delta Like 4 Expressing Bone Marrow-Derived Endothelial Progenitor Cells Regulate Tumour Angiogenesis." Blood 110, no. 11 (November 16, 2007): 3728. http://dx.doi.org/10.1182/blood.v110.11.3728.3728.

Full text
Abstract:
Abstract Bone marrow-derived endothelial progenitor cells (BM-EPCs) have been implicated in adult neoangiogenesis and consequently used as therapies for human pathologies with endothelial damage. The administration of these cells in human patients temporally improves endothelial function, although the engraftment of these cells in newly formed vessels is inefficient. Conversely, therapeutic stratagies to block EPC contribution during tumor angiogenesis have been proposed. In this work, we analysed the role of the Notch/Delta signalling pathway in EPC function during tumour neoangiogenesis, by regulating the expression of Notch ligand, delta-like 4 (Dll4) in these cells. Sublethally irradiated NOD-SCID mice received WT, Dll4+/− (Dll4 heterozygous mice) or Dll4 SiRNA-treated BM-EPCs and were subcutaneously inoculated with well established Human or murine tumor xenografts. Tumours growing in Dll4-depleted EPCs transplanted mice presented increased microvessel density when compared with WT EPCs transplanted mice or non-transplanted controls, regardless of VEGF expression. Although with increased vessel number, tumours of Dll4+/− EPC transplanted mice presented increased hypoxia and decreased tumour cell proliferation, suggesting an impairment in vessel function. In addition, these tumours present a diminished expression of PDGF, a vessel stabilizing factor, and increased expression of Ang2, known as a vessel destabilizing factor. We next verified whether the vessel destabilization observed in tumors after Dll4-depleted EPCs transplant might be due to a diferential endothelial differentiation or incorporation of EPCs in the tumour vasculature. In order to answer this question we quantified the incorporation of WT and Dll4-depleted EPCs in tumour vessels. Accordingly to our results, the presence of Dll4-depleted EPCs was reduced compared to WT EPCs, suggesting that Dll4-depleted EPCs might have reduced capacity to adhere to the renewing tumor vasculature, or to the underlying basement membrane. To test this, we used an in vitro endothelial differentiation assay, and observed a defect on the adhesion of of Dll4-depleted EPCs to extracellular matrix, which was correlated with a reduced expression of integrin subunits a3 and b1. These results suggest that the reduction of Dll4 on EPCs reduces integrin expression interfering with their ability to adhere, incorporate and stabilize the tumor vasculature during tumor neoangiogenesis. Therefore, EPCs have a major role in vessel stabilization in active neoangiogenic sites by the regulation of Dll4 expression. We propose that targeting the Notch/Dll4 pathway on EPCs, modulating vessel stability, may have therapeutic potential.
APA, Harvard, Vancouver, ISO, and other styles
6

Schröder, Sabine, Simone Broese, Jana Baake, Dajana Juerß, Stephan Kriesen, Guido Hildebrandt, and Katrin Manda. "Effect of Ionizing Radiation on Human EA.hy926 Endothelial Cells under Inflammatory Conditions and Their Interactions with A549 Tumour Cells." Journal of Immunology Research 2019 (September 2, 2019): 1–14. http://dx.doi.org/10.1155/2019/9645481.

Full text
Abstract:
Purpose. Most tumours are characterized by an inflammatory microenvironment, and correlations between inflammation and cancer progression have been shown. Endothelial cells (ECs), as part of the tumour microenvironment, play a crucial role in inflammatory processes as well as in angiogenesis and could be critical targets of cancer therapy like irradiation. Therefore, in the present study we investigated the effect of ionizing radiation on endothelial cells under inflammatory conditions and their interactions with tumour cells. Methods. Nonactivated and TNF-α treatment-activated human EC EA.hy926 were irradiated with doses between 0.1 Gy and 6 Gy with a linear accelerator. Using a multiplex assay, the accumulation of various chemokines (IL-8, MCP-1, E-selectin, and P-selectin) and soluble adhesion molecules (sICAM-1 and VCAM-1) as well as protein values of the vascular endothelial growth factor (VEGF) was measured in the supernatant at different time points. The adhesion capability of irradiated and nonirradiated A549 tumour cells to EA.hy926 cells was measured using flow cytometry, and the migration of tumour cells was investigated with a scratch motility assay. Results. In contrast to unirradiated cells, IR of ECs resulted in a modified release of chemokines IL-8 and MCP-1 as well as the adhesion molecules sICAM-1 and VCAM-1 in the EC, whereas concentrations of E-selectin and P-selectin as well as VEGF were not influenced. IR always affected the adhesion capability of tumour cells to ECs with the effect dependent on the IR-treated cell type. TNF-α treatment generally increased adhesion ability of the tumour cells. Tumour cell migration was clearly inhibited after IR. This inhibitory effect was eliminated for radiation doses from 0.5 to 2 Gy when, additionally, an inflammatory environment was predominant. Conclusions. Our results support past findings suggesting that ECs, as part of the inflammatory microenvironment of tumours, are important regulators of the actual tumour response to radiation therapy.
APA, Harvard, Vancouver, ISO, and other styles
7

Bordon, Yvonne. "Macrophages throw tumour cells a lifeline." Nature Reviews Immunology 19, no. 4 (March 5, 2019): 202–3. http://dx.doi.org/10.1038/s41577-019-0148-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Ashman, Leonie K. "The immunogenicity of tumour cells." Immunology and Cell Biology 65, no. 4 (August 1987): 271–77. http://dx.doi.org/10.1038/icb.1987.31.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Carpenter, Ben, Sara Ghorashian, Emma Nicholson, James Edward Griffin, Maryam Ahmadi, Angelika Holler, Barry Flutter, et al. "Targeting Therapeutic T Cells to Tumour Niches." Blood 120, no. 21 (November 16, 2012): 3009. http://dx.doi.org/10.1182/blood.v120.21.3009.3009.

Full text
Abstract:
Abstract Abstract 3009 Background: Interactions between tumour cells and host cells within the microenvironment are important in promoting the development of cancer. Tumor niches provide crucial anti-apoptotic and anti-proliferative signals that drive tumor chemoresistance. The CXCR4-CXCL12 chemokine axis forms a critical component of this niche. CXCL12 produced by stromal cells has direct pro-survival effects upon tumor cells, promotes metastasis and recruits CXCR4-expressing regulatory T cell populations that block anti-tumour immunity. In this study, we have tested the hypothesis that targeting therapeutic T cells to CXCR4-dependent niches will improve eradication of tumours in mice. Methods: The murine CXCR4 gene was inserted into retroviral vector, pMP71. Murine T cells were transduced with CXCR4 or control vector and tested for homing in vitro to CXCL12 through chemotaxis assays. In vivo imaging of the putative endosteal bone marrow (BM) niche was performed by multiphoton imaging through cranial frontal bones in osteoblast (collagen 1-α-GFP) reporter mice. In vivo trafficking, competitive transfer and memory recall experiments were performed following transfer of transduced T cells to syngeneic, sub-lethally irradiated mice. Anti-tumour reactivity of CXCR4-transduced T cells was tested in models of allogeneic BM transplantation (BMT). Results: CXCR4-transduced T cells demonstrated enhanced migration towards CXCL12 in vitro. No differences in viability, phenotype or function were observed in CXCR4-transduced versus control T cells in the presence or absence of CXCL12. In competitive assays, CXCR4-transduced CD8 T cells demonstrated a 2-fold greater capacity than controls to home to the BM by 24h after transfer to sub-lethally-irradiated recipients. Multiphoton imaging through cranial frontal bones indicated that fluorescently labelled CXCR4-transduced T cells were closer than control cells to the endosteum (13 μm versus 17 μm, p<0.01). By 14 days, the numbers of CXCR4-transduced CD8 T cells in the BM were 15-fold greater than controls. To test immunity to model antigen, CXCR4 or control vector-transduced OT-1 TCR-transgenic CD8 cells were transferred to sub-lethally irradiated mice before challenge with OVA peptide-loaded dendritic cells. Pre-vaccination, CXCR4-transduced OT-1 cells demonstrated greater engraftment than controls in the BM and spleen. Seven days following vaccination, CXCR4 OT-1 cells demonstrated a greater capacity than control cells to generate IFN-γ to OVA-peptide. Four weeks following vaccination, CXCR4-transduced CD8 T cells showed increased frequencies of cells with a CD44highIL-7Rαhigh memory phenotype than controls, with a greater proportion of cells undergoing proliferation as evaluated by BrdU incorporation. To test T cell immunity against a tumor that exploits the CXCR4-CXCL12 axis to recruit regulatory T cells, B6 BM and CXCR4- or control transduced B6 T cells were transferred to irradiated BALB/c recipients given A20 tumor. Tumor growth was delayed to a greater extent following transfer of CXCR4-compared to control-transduced donor T cells. Conclusion: Over-expression of CXCR4 in CD8 T cells potentiates engraftment, initial effector function and generation of memory cells. Disclosures: Stauss: Cell Medica: Scientific Advisor Other.
APA, Harvard, Vancouver, ISO, and other styles
10

Battke, Christina, Romana Ruiss, Ulrich Welsch, Pauline Wimberger, Stephan Lang, Simon Jochum, and Reinhard Zeidler. "Tumour exosomes inhibit binding of tumour-reactive antibodies to tumour cells and reduce ADCC." Cancer Immunology, Immunotherapy 60, no. 5 (February 4, 2011): 639–48. http://dx.doi.org/10.1007/s00262-011-0979-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
11

Gasser, Stephan, Lina H. K. Lim, and Florence S. G. Cheung. "The role of the tumour microenvironment in immunotherapy." Endocrine-Related Cancer 24, no. 12 (December 2017): T283—T295. http://dx.doi.org/10.1530/erc-17-0146.

Full text
Abstract:
Recent success in immunomodulating strategies in lung cancer and melanoma has prompted much enthusiasm in their potential to treat other advanced solid malignancies. However, their applications have shown variable success and are even ineffective against some tumours. The efficiency of immunotherapies relies on an immunogenic tumour microenvironment. The current field of cancer immunology has focused on understanding the interaction of cancer and host immune cells to break the state of immune tolerance and explain how molecular patterns of cytokines and chemokines affect tumour progression. Here, we review our current knowledge of how inherent properties of tumours and their different tumour microenvironments affect therapeutic outcome. We also discuss insights into recent multimodal therapeutic approaches that target tumour immune evasion and suppression to restore anti-tumour immunity.
APA, Harvard, Vancouver, ISO, and other styles
12

Ishida, A., H. Tanaka, T. Hiura, S. Miura, S. Watanabe, K. Matsuyama, H. Kuriyama, et al. "Generation of Anti-tumour Effector T Cells from Naïve T Cells by Stimulation with Dendritic/tumour Fusion Cells." Scandinavian Journal of Immunology 66, no. 5 (November 2007): 546–54. http://dx.doi.org/10.1111/j.1365-3083.2007.02012.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
13

Zou, Weiping, and Nicholas P. Restifo. "TH17 cells in tumour immunity and immunotherapy." Nature Reviews Immunology 10, no. 4 (April 2010): 248–56. http://dx.doi.org/10.1038/nri2742.

Full text
APA, Harvard, Vancouver, ISO, and other styles
14

Knight, Stella C. "Dendritic cells as initiators of tumour immunity." Immunology Today 16, no. 11 (November 1995): 547. http://dx.doi.org/10.1016/0167-5699(95)80050-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
15

LAW, S. K. A. "Antigen shedding and metastasis of tumour cells." Clinical & Experimental Immunology 85, no. 1 (June 28, 2008): 1–2. http://dx.doi.org/10.1111/j.1365-2249.1991.tb05672.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
16

Ward, Stephen, David Casey, Marie-Christine Labarthe, Michael Whelan, Angus Dalgleish, Hardev Pandha, and Stephen Todryk. "Immunotherapeutic potential of whole tumour cells." Cancer Immunology, Immunotherapy 51, no. 7 (June 14, 2002): 351–57. http://dx.doi.org/10.1007/s00262-002-0286-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
17

Ogino, Shuji, Jonathan A. Nowak, Tsuyoshi Hamada, Amanda I. Phipps, Ulrike Peters, Danny A. Milner Jr, Edward L. Giovannucci, et al. "Integrative analysis of exogenous, endogenous, tumour and immune factors for precision medicine." Gut 67, no. 6 (February 6, 2018): 1168–80. http://dx.doi.org/10.1136/gutjnl-2017-315537.

Full text
Abstract:
Immunotherapy strategies targeting immune checkpoints such as the CTLA4 and CD274 (programmed cell death 1 ligand 1, PD-L1)/PDCD1 (programmed cell death 1, PD-1) T-cell coreceptor pathways are revolutionising oncology. The approval of pembrolizumab use for solid tumours with high-level microsatellite instability or mismatch repair deficiency by the US Food and Drug Administration highlights promise of precision immuno-oncology. However, despite evidence indicating influences of exogenous and endogenous factors such as diet, nutrients, alcohol, smoking, obesity, lifestyle, environmental exposures and microbiome on tumour-immune interactions, integrative analyses of those factors and immunity lag behind. Immune cell analyses in the tumour microenvironment have not adequately been integrated into large-scale studies. Addressing this gap, the transdisciplinary field of molecular pathological epidemiology (MPE) offers research frameworks to integrate tumour immunology into population health sciences, and link the exposures and germline genetics (eg, HLA genotypes) to tumour and immune characteristics. Multilevel research using bioinformatics, in vivo pathology and omics (genomics, epigenomics, transcriptomics, proteomics and metabolomics) technologies is possible with use of tissue, peripheral blood circulating cells, cell-free plasma, stool, sputum, urine and other body fluids. This immunology-MPE model can synergise with experimental immunology, microbiology and systems biology. GI neoplasms represent exemplary diseases for the immunology-MPE model, given rich microbiota and immune tissues of intestines, and the well-established carcinogenic role of intestinal inflammation. Proof-of-principle studies on colorectal cancer provided insights into immunomodulating effects of aspirin, vitamin D, inflammatory diets and omega-3 polyunsaturated fatty acids. The integrated immunology-MPE model can contribute to better understanding of environment-tumour-immune interactions, and effective immunoprevention and immunotherapy strategies for precision medicine.
APA, Harvard, Vancouver, ISO, and other styles
18

Hokland, Marianne, Mikkel S. Petersen, Charlotte C. Fleischer, Hans Stødkilde-Jørgensen, Søren B. Hansen, Ulrik Skands, Hans J. G. Gundersen, and Ralf Agger. "Tumor Localization and Quantitation of Adoptively Transfered T Lymphocytes in a Murine Model." Blood 104, no. 11 (November 16, 2004): 1343. http://dx.doi.org/10.1182/blood.v104.11.1343.1343.

Full text
Abstract:
Abstract Tracking adoptively transferred antigen-specific T lymphocytes is an important prerequisite for devising better protocols for cellular therapy. To this end we have developed a highly sensitive method for “in situ” visualization of labelled lymphocytes in vivo by combined PET and magnetic resonance imaging (MRI) to monitor the distribution of adoptively transferred tumour-specific T cells in a mouse model system. Moreover, quantitation of the adoptively transferred cells in tumor was performed by flow cytometry. C57BL/6J mice carrying subcutaneous tumours of the ovalbumin (OVA)-expressing malignant melanoma cell line B16-OVA were adoptively transferred with OVA-specific CD8+ T cells labelled with 124IdU. Five days after transfer of T cells, mice were killed and subjected to PET and MR imaging. Using a newly developed method for co-registration of the two image modalities, the anatomical localisation of the transferred cells was visualised and the amount of radioactivity in various anatomical locations very accurately determined. For quantitation of tumor infiltrating non-labelled OVA-specific CD8+ T cells by flow cytometry (using AbsoluteCount Beads), tumors were removed from mice day 1 until day 8 following adoptive transfer (6 mice/group) and prepared for single cell suspension before labeled with anti-CD8-FITC and SIINFEKL-Tetramer-PE. Results showed a clear tumor localization of the adoptively transferred OVA-specific T cells in the tumours. In two independent experiments comprising 12 and 13 evaluable mice, respectively, we found a mean value of 0.909 +/− 0.468 Bq and 0.926 +/− 0.553 Bq in the tumours, and only 0.182 +/− 0.479 Bq and 0.026 +/− 0.480 Bq in the corresponding contralateral control volumes. The difference in activity between the tumour regions and the control regions was statistically highly significant with 2p-values of 0.002 and 0.006 for the two experiments. Using flow cytometry it was shown that the number of OVA specific T lymphocytes accumulating in tumor gradually increased until day 5 after transfer when an average of 3.3 million SIINFEKL-specific cells per gram tumor tissue was found. From day 5 until day 8 the number of SIINFEKL-specific cells per gram tumor tissue fluctuated at a fairly constant level. This method presented for tracking adoptively transfered tumor specific T lymphocytes represent a significant advancement for studies of adoptively transferred specific T cells, and could potentially be developed for diagnostic purposes. Moreover, since these studies show that tumor-specific T cells home to subcutaneous tumours in substantial numbers, we suggest that these migrating cells could be employed in a new form of therapy as carriers of toxic substances to tumors.
APA, Harvard, Vancouver, ISO, and other styles
19

Sharonov, George V., Ekaterina O. Serebrovskaya, Diana V. Yuzhakova, Olga V. Britanova, and Dmitriy M. Chudakov. "B cells, plasma cells and antibody repertoires in the tumour microenvironment." Nature Reviews Immunology 20, no. 5 (January 27, 2020): 294–307. http://dx.doi.org/10.1038/s41577-019-0257-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
20

Le Pape, A., C. Jubault, R. Barot-Clorbaru, M. Musset, and G. Mathé. "Targetting of immunocompetent cells for tumour scintigraphy." International Journal of Immunopharmacology 10 (January 1988): 29. http://dx.doi.org/10.1016/0192-0561(88)90229-9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
21

Soars, Diane, Angus G. Dalgleish, Alan A. Melcher, Hardev S. Pandha, Stephen M. Todryk, Jonathan Eaton, Lindsay Birchall, and Rebecca Greenhalgh. "Heated tumour cells of autologous and allogeneic origin elicit anti-tumour immunity." Cancer Immunology, Immunotherapy 53, no. 4 (April 1, 2004): 323–30. http://dx.doi.org/10.1007/s00262-003-0452-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
22

Mahnke, Yolanda D., Jochen Schwendemann, Philipp Beckhove, and Volker Schirrmacher. "Maintenance of long-term tumour-specific T-cell memory by residual dormant tumour cells." Immunology 115, no. 3 (July 2005): 325–36. http://dx.doi.org/10.1111/j.1365-2567.2005.02163.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
23

Minton, Kirsty. "B cells lead the way in tumour progression." Nature Reviews Immunology 5, no. 7 (June 20, 2005): 517. http://dx.doi.org/10.1038/nri1653.

Full text
APA, Harvard, Vancouver, ISO, and other styles
24

Zou, Weiping, and Nicholas P. Restifo. "Erratum: TH17 cells in tumour immunity and immunotherapy." Nature Reviews Immunology 11, no. 8 (July 25, 2011): 565. http://dx.doi.org/10.1038/nri3029.

Full text
APA, Harvard, Vancouver, ISO, and other styles
25

Jackson, Andrew M., M. A. Chambers, P. J. Selby, and G. Packham. "Apoptosis of tumour cells during infection with mycobacteria." Immunology Letters 56 (May 1997): 444. http://dx.doi.org/10.1016/s0165-2478(97)86805-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
26

Raffaghello, Lizzia, and Francesco Dazzi. "Classification and biology of tumour associated stromal cells." Immunology Letters 168, no. 2 (December 2015): 175–82. http://dx.doi.org/10.1016/j.imlet.2015.06.016.

Full text
APA, Harvard, Vancouver, ISO, and other styles
27

Gottfried, E., M. Kreutz, S. Haffner, E. Holler, M. Iacobelli, R. Andreesen, and G. Eissner. "Differentiation of Human Tumour-associated Dendritic Cells into Endothelial-like Cells: An Alternative Pathway of Tumour Angiogenesis." Scandinavian Journal of Immunology 65, no. 4 (April 2007): 329–35. http://dx.doi.org/10.1111/j.1365-3083.2007.01903.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
28

Vauleon, Elodie, Tony Avril, Brigitte Collet, Jean Mosser, and Véronique Quillien. "Overview of Cellular Immunotherapy for Patients with Glioblastoma." Clinical and Developmental Immunology 2010 (2010): 1–18. http://dx.doi.org/10.1155/2010/689171.

Full text
Abstract:
High grade gliomas (HGG) including glioblastomas (GBM) are the most common and devastating primary brain tumours. Despite important progresses in GBM treatment that currently includes surgery combined to radio- and chemotherapy, GBM patients' prognosis remains very poor. Immunotherapy is one of the new promising therapeutic approaches that can specifically target tumour cells. Such an approach could also maintain long term antitumour responses without inducing neurologic defects. Since the past 25 years, adoptive and active immunotherapies using lymphokine-activated killer cells, cytotoxic T cells, tumour-infiltrating lymphocytes, autologous tumour cells, and dendritic cells have been tested in phase I/II clinical trials with HGG patients. This paper inventories these cellular immunotherapeutic strategies and discusses their efficacy, limits, and future perspectives for optimizing the treatment to achieve clinical benefits for GBM patients.
APA, Harvard, Vancouver, ISO, and other styles
29

Byrne, Scott N., and Gary M. Halliday. "Dendritic cells: Making progress with tumour regression?" Immunology and Cell Biology 80, no. 6 (December 2002): 520–30. http://dx.doi.org/10.1046/j.1440-1711.2002.01122.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
30

Albertsson, Per A., Per H. Basse, Marianne Hokland, Ronald H. Goldfarb, J. Fred Nagelkerke, Ulf Nannmark, and Peter J. K. Kuppen. "NK cells and the tumour microenvironment: implications for NK-cell function and anti-tumour activity." Trends in Immunology 24, no. 11 (November 2003): 603–9. http://dx.doi.org/10.1016/j.it.2003.09.007.

Full text
APA, Harvard, Vancouver, ISO, and other styles
31

Semiglazov, V. F., A. I. Tseluiko, I. A. Baldueva, T. L. Nekhaeva, A. S. Artemyeva, A. G. Kudaybergenova, S. A. Protsenko, et al. "Immunology and immunotherapy in the complex treatment of malignant tumors." Meditsinskiy sovet = Medical Council, no. 4 (April 20, 2021): 248–57. http://dx.doi.org/10.21518/2079-701x-2021-4-248-257.

Full text
Abstract:
Immuno-oncology is a rapidly developing field in medicine. Drug combination therapies have already been studied in many clinical trials of different types of tumours. In recent years, a checkpoint inhibition therapy with monoclonal antibodies that target cytological T-lymphocytes has been developed. Thus, inhibition of two regulator genes CTLA 4 and PD1 or PD-L1 ligand to it is able to restore mediated T-cell tumour regression in its many localizations. The article considers a number of key fields of immunology and immunotherapy through a specific example of breast cancer (BC): the role of T-lymphocytes, vaccines, biomarkers of immunotherapy. The treatment used by the authors was based on an innovative technology of autologous dendritic cell-based vaccine based on highly immunogenic cancer/testis antigens (CTA) for immunotherapy of malignant tumours. The technology of specific CTA+-activated autologous dendritic cells (DC)-based immunotherapy was chosen as an innovative solution for the treatment of breast cancer patients. The treatment results showed that a clinically significant anti-tumour effect was achieved in 73.7% of patients. Median disease-free survival was 8.3 months (95% Cl 6.5-9.9 months), no grade 3-4 complications were recorded, grade 1-2 complications were observed in 57% of patients. The immunological effect in laboratory tests was recorded in 92% of patients. Thus, autologous DCs loaded with cancer/testis antigens can be considered as palliative dendritic vaccine therapy in patients with metastatic breast cancer who have exhausted standard treatment options. Also, the authors presented the results of immunological studies of the prognostic and predictive significance of the immunological response from the perspective of pathomorphology and general immunology, including tumour-infiltrating T-lymphocytes (TILs, CD3, CD4, CD8), their quantitative ratio and correlation with regulatory genes (PD-1, PD- L1, FOX-P3). The results of overall analysis comprising data of 2,148 patients from 9 centers confirmed the strong prognostic role of stromal tumour-infiltrating lymphocytes (sTILs) in early triple-negative breast cancer.
APA, Harvard, Vancouver, ISO, and other styles
32

Redzovic, Arnela, Gordana Laskarin, Marin Dominovic, Herman Haller, and Daniel Rukavina. "Mucins Help to Avoid Alloreactivity at the Maternal Fetal Interface." Clinical and Developmental Immunology 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/542152.

Full text
Abstract:
During gestation, many different mechanisms act to render the maternal immune system tolerant to semi-allogeneic trophoblast cells of foetal origin, including those mediated via mucins that are expressed during the peri-implantation period in the uterus. Tumour- associated glycoprotein-72 (TAG-72) enhances the already established tolerogenic features of decidual dendritic cells with the inability to progress towards Th1 immune orientation due to lowered interferon (IFN)-γand interleukin (IL)-15 expression. Mucine 1 (Muc 1) supports alternative activation of decidual macrophages, restricts the proliferation of decidual regulatory CD56+bright natural killer (NK) cells, and downregulates their cytotoxic potential, including cytotoxic mediator protein expression. Removing TAG-72 and Muc 1 from the eutopic implantation site likely contributes to better control of trophoblast invasion by T cells and NK cells and appears to have important immunologic advantages for successful implantation, in addition to mechanical advantages. However, these processes may lead to uncontrolled trophoblast growth after implantation, inefficient defence against infection or tumours, and elimination of unwanted immunocompetent cells at the maternal-foetal interface. The use of mucins by tumour cells to affect the local microenvironment in order to avoid the host immune response and to promote local tumour growth, invasion, and metastasis confirms this postulation.
APA, Harvard, Vancouver, ISO, and other styles
33

Sapega, O., R. Mikyskova, K. Musilek, J. Bieblova, Z. Hodny, and M. Reinis. "P01.16 Effects of the STAT3 inhibitors on senescent tumour cells." Journal for ImmunoTherapy of Cancer 8, Suppl 2 (October 2020): A16.1—A16. http://dx.doi.org/10.1136/jitc-2020-itoc7.29.

Full text
Abstract:
BackgroundCellular senescence is the process of cell proliferation arrest. Premature cellular senescence can be induced by chemotherapy, irradiation and, under certain circumstances, by cytokines. Senescent cells produce a number of secreted proteins and growth factors that may either stimulate or inhibit cell proliferation. One of the major cytokines that play role in regulation of cellular senescence is IL-6. IL-6/STAT3 signaling pathway represent decisive regulatory factors in cellular senescence. The objective of this study was to compare the effects of the STAT3 inhibitors on senescent and proliferative tumour cells. Further, the therapeutic potential of the STAT3 inhibitors was evaluated using murine tumour models.Materials and MethodsIn vitro, as well as in vivo experiments were performed using TC-1 (model for HPV16-associated tumours) TRAMP-C2 (prostate cancer) cell lines. C57Bl/6NCrl mice, 7–8 weeks old, were obtained from Velaz (Prague, Czech Republic). Experimental protocols were approved by the Institutional Animal Care Committee of the Institute of Molecular Genetics (Prague, Czech Republic). STAT3 inhibitors, namely STATTIC, BP-102 (synthesised at the University of Hradec Kralove) and their derivatives were tested for their effects on tumour cells, such as cytotoxicity, ability to inhibit STAT3 phosphorylation, cell proliferation and tumour growth in syngeneic mice.ResultsWe have previously demonstrated that docetaxel-induced senescence in the TC-1 and TRAMP-C2 murine tumour cell lines, which was proved by in vitro (detection of increased p21 expression, positive beta-galactosidase staining, and the typical SASP capable to induce ‘bystander’ senescence), and in vivo experiments, using C57BL/6 mice [1]. Both TC-1 and TRAMP-C2 cells displayed elevated IL-6 secretion and activated STAT3 signaling pathway. Therefore, we tested efficacy of the STAT3 inhibitors on these cell lines. Cytotoxic and STAT3 phosphorylation inhibitory effects of the inhibitors were observed in both proliferating and senescent cells. Antitumor effects of selected inhibitors were evaluated.ConclusionsCollectively, STAT3 is an attractive target for therapeutic approaches in cancer treatment and we can assume that inhibition of the STAT3 pathway can be used for elimination of the pernicious effects of the senescent cells.ReferenceSimova J, Sapega O, Imrichova T, Stepanek I, Kyjacova L, Mikyskova R, Indrova M, Bieblova J, Bubenik J, Bartek J, et al: Tumor growth accelerated by chemotherapy-induced senescent cells is suppressed by treatment with IL-12 producing cellular vaccines. Oncotarget7: 54952–54964, 2016. This work was supported by the research grant No. NV18-05-00562 provided by the Grant Agency of the Ministry of Health of the Czech Republic.Disclosure InformationO. Sapega: None. R. Mikyskova: None. K. Musilek: None. J. Bieblova: None. Z. Hodny: None. M. Reinis: None.
APA, Harvard, Vancouver, ISO, and other styles
34

Turley, Shannon J., Viviana Cremasco, and Jillian L. Astarita. "Immunological hallmarks of stromal cells in the tumour microenvironment." Nature Reviews Immunology 15, no. 11 (October 16, 2015): 669–82. http://dx.doi.org/10.1038/nri3902.

Full text
APA, Harvard, Vancouver, ISO, and other styles
35

Schmidt-Arras, Dirk, Eithan Galun, and Stefan Rose-John. "The two facets of gp130 signalling in liver tumorigenesis." Seminars in Immunopathology 43, no. 4 (May 28, 2021): 609–24. http://dx.doi.org/10.1007/s00281-021-00861-0.

Full text
Abstract:
AbstractThe liver is a vital organ with multiple functions and a large regenerative capacity. Tumours of the liver are the second most frequently cause of cancer-related death and develop in chronically inflamed livers. IL-6-type cytokines are mediators of inflammation and almost all members signal via the receptor subunit gp130 and the downstream signalling molecule STAT3. We here summarize current knowledge on how gp130 signalling and STAT3 in tumour cells and cells of the tumour micro-environment drives hepatic tumorigenesis. We furthermore discuss very recent findings describing also anti-tumorigenic roles of gp130/STAT3 and important considerations for therapeutic interventions.
APA, Harvard, Vancouver, ISO, and other styles
36

Matos Pires, Eugénia, and Cecília Moura. "Immune Response in Melanoma: A Basis to Understand the Role of Immunotherapy with Immune Checkpoint Inhibitors." Journal of the Portuguese Society of Dermatology and Venereology 76, no. 1 (April 5, 2018): 47–52. http://dx.doi.org/10.29021/spdv.76.1.868.

Full text
Abstract:
The knowledge of the pathophysiology of tumour progression is crucial to understand the therapeutic targets in order to control the disease. The mechanisms used by the immune system to affect cancer development and progression has been a challenging question in immunology. It is now postulated that immunology plays a dual role in this process: it protects against tumour growth, destroying “aberrant” tumour cells, but may also promote tumour progression by selecting tumour cells that are able to escape the immune response and survive in an immunocompetent host. These findings gave rise to the concept of “cancer immunoediting”, which explains the influence of the immune system on tumour progression. Several observations like immunosuppression as a risk factor for melanoma, the possibility of partial or complete regression of primary tumour and development of vitiligo, have suggested that melanoma is an immunogenic tumour but a successful tumour evolution can occur in the light of the “immunoediting” concept. Immune checkpoints, cytotoxic T lymphocyte antigen (CTLA)-4 and programmed cell death (PD-1), were recognized to have important roles in regulating T cell responses during tumour development and were proven to be effective targets in treating advanced melanoma. This article will briefly review the process of tumour evolution and its interaction with the immune system as well as the mechanism of action of the immune checkpoint inhibitors to understand better the new targeted immunotherapies for advanced melanoma, that will be further discussed.
APA, Harvard, Vancouver, ISO, and other styles
37

Hacker, Ulrich T., Ines Schildhauer, Margarita C. Barroso, David M. Kofler, Franz M. Gerner, Josef Mysliwietz, Hildegard Buening, Michael Hallek, and Susan B. S. King. "Gene transfer preferentially selects MHC class I positive tumour cells and enhances tumour immunogenicity." Cancer Immunology, Immunotherapy 55, no. 5 (July 26, 2005): 547–57. http://dx.doi.org/10.1007/s00262-005-0035-4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
38

Hughes, Ellyn, Sarah N. Lauder, Kathryn Smart, Anja Bloom, Jake Scott, Emma Jones, Michelle Somerville, et al. "Primary breast tumours but not lung metastases induce protective anti-tumour immune responses after Treg-depletion." Cancer Immunology, Immunotherapy 69, no. 10 (May 23, 2020): 2063–73. http://dx.doi.org/10.1007/s00262-020-02603-x.

Full text
Abstract:
Abstract Although metastatic disease is responsible for the majority of cancer deaths, tests of novel immunotherapies in mouse tumour models often focus on primary tumours without determining whether these therapies also target metastatic disease. This study examined the impact of depleting Foxp3+ regulatory T cells (Treg), on lung metastases, using a mouse model of breast cancer. After Treg-depletion, generation of an immune response to the primary tumour was a critical determinant for limiting development of metastasis. Indeed, resection of the primary tumour abrogated any effect of Treg-depletion on metastases. In addition, whilst the immune response, generated by the primary tumour, prevented metastases development, it had little impact on controlling established disease. Collectively, the data indicate that metastatic cells in the lung are not controlled by immune responses induced by the primary tumour. These findings indicate that targeting Tregs alone will not suffice for treating lung metastases.
APA, Harvard, Vancouver, ISO, and other styles
39

Mulder, Wilhelmina M. C., Marij J. Stukart, Micha Roos, Ren� A. W. van Lier, John Wagstaff, R. J. Scheper, and E. Bloemena. "Culture of tumour-infiltrating lymphocytes from melanoma and colon carcinoma: removal of tumour cells does not affect tumour-specificity." Cancer Immunology, Immunotherapy 41, no. 5 (December 1, 1995): 293–301. http://dx.doi.org/10.1007/s002620050231.

Full text
APA, Harvard, Vancouver, ISO, and other styles
40

Mulder, Wilhelmina M. C., Marij J. Stukart, Micha Roos, René A. W. van Lier, John Wagstaff, Rik J. Scheper, and Elisabeth Bloemena. "Culture of tumour-infiltrating lymphocytes from melanoma and colon carcinoma: Removal of tumour cells does not affect tumour-specificity." Cancer Immunology, Immunotherapy 41, no. 5 (September 1995): 293–301. http://dx.doi.org/10.1007/bf01517217.

Full text
APA, Harvard, Vancouver, ISO, and other styles
41

Du Toit, Andrea. "Tumour cells show off bacterial peptides." Nature Reviews Microbiology 19, no. 5 (March 25, 2021): 284. http://dx.doi.org/10.1038/s41579-021-00551-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
42

Shklovskaya, Elena, Alexandra M. Terry, Thomas V. Guy, Adrian Buckley, Holly A. Bolton, Erhua Zhu, Jeff Holst, and Barbara Fazekas de St Groth. "Tumour‐specific CD4 T cells eradicate melanoma via indirect recognition of tumour‐derived antigen." Immunology & Cell Biology 94, no. 6 (March 2016): 593–603. http://dx.doi.org/10.1038/icb.2016.14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
43

Fares, Jawad, Ilya Ulasov, Peter Timashev, and Maciej S. Lesniak. "Emerging principles of brain immunology and immune checkpoint blockade in brain metastases." Brain 144, no. 4 (April 1, 2021): 1046–66. http://dx.doi.org/10.1093/brain/awab012.

Full text
Abstract:
Abstract Brain metastases are the most common type of brain tumours, harbouring an immune microenvironment that can in principle be targeted via immunotherapy. Elucidating some of the immunological intricacies of brain metastases has opened a therapeutic window to explore the potential of immune checkpoint inhibitors in this globally lethal disease. Multiple lines of evidence suggest that tumour cells hijack the immune regulatory mechanisms in the brain for the benefit of their own survival and progression. Nonetheless, the role of the immune checkpoint in the complex interplays between cancers cells and T cells and in conferring resistance to therapy remains under investigation. Meanwhile, early phase trials with immune checkpoint inhibitors have reported clinical benefit in patients with brain metastases from melanoma and non-small cell lung cancer. In this review, we explore the workings of the immune system in the brain, the immunology of brain metastases, and the current status of immune checkpoint inhibitors in the treatment of brain metastases.
APA, Harvard, Vancouver, ISO, and other styles
44

HARRIS, C. L., K. S. KAN, G. T. STEVENSON, and B. P. MORGAN. "Tumour cell killing using chemically engineered antibody constructs specific for tumour cells and the complement inhibitor CD59." Clinical & Experimental Immunology 107, no. 2 (February 1997): 364–71. http://dx.doi.org/10.1111/j.1365-2249.1997.265-ce1156.x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
45

Gaken, Joop, Louisa Pericleous, Farzin Farzaneh, Ghulam J. Mufti, and Mahvash Tavassoli. "TAT-Apoptin Mediated Induction of Apoptosis in Leukaemic Cells." Blood 108, no. 11 (November 16, 2006): 1900. http://dx.doi.org/10.1182/blood.v108.11.1900.1900.

Full text
Abstract:
Abstract We have studied the specific targeting of leukaemic cells using the Chicken Anaemia Virus (CAV)-derived protein VP3 (Apoptin) linked to the protein transduction domain (PTD) from HIV TAT with the aim of using this strategy for in vitro purging. Apoptin is a 13.6 kDa protein which induces apoptosis specifically in cancer cells whilst leaving normal cells unaffected. Expression of Apoptin in normal cells results in its cytoplasmic localisation. In tumour cells Apoptin resides initially in the cytoplasm and subsequently translocates to the nucleus and induces apoptosis. Apoptin is phosphorylated both in vitro and in vivo in tumour cells but negligibly in normal cells at threonine 108. A gain-of-function point mutation (T108E) results in accumulation of Apoptin in the nucleus and the killing of normal cells, implying that phosphorylation is a key factor of the tumour-specific properties of Apoptin. We have demonstrated that Apoptin induces apoptosis in a variety of human solid tumour cell lines, but not in normal fibroblast and epithelial cells. Apoptin induced apoptosis in HSC3 head and neck cancer cells acts through the mitochondrial pathway and was blocked (>75%) by shRNA against PUMA, a BH3 Only protein which induces Bax and BAK resulting in loss of mitochondrial membrane potential and release of cytochrome C. Furthermore, activation of the p53 family member, p73, substantially increased (5–10 fold for p73 β and γ) sensitivity of Saos2 tumour cells to Apoptin-induced killing. For efficient protein delivery, Apoptin was fused to a TAT PTD and addition of this protein to normal and tumour cells resulted in the selective killing of tumour cells. To increase the stability and solubility of TAT-Apoptin we have fused it to the maltose binding protein (MBP), this modification significantly increases both yield and the solubility of Apoptin while retaining its biological function. Apoptin tumour specific toxicity was assessed in a range of leukaemic and solid tumour cell lines. Addition of MBP-TAT-Apoptin protein to HL60, K562 and Jurkat cells resulted in 50%, 55% and 75% cell death by apoptosis as judged by PARP cleavage, respectively, at day 4 as compared to MBP-TAT control whilst normal B cells, fibroblasts and epithelial cells are unaffected. Fluorescent microscopy demonstrated that MBP-TAT-Apoptin was rapidly internalised in almost 100% of cells within 24hrs in all cell types tested. Direct injection of Apoptin expressing Ad vectors also showed clear regression of established tumours in mice. The cancer specific toxicity of Apoptin has potential value for a range of therapeutic applications such as purging of autologous bone marrow as used for the treatment of multiple myeloma and possibly direct treatment of leukaemias either alone or linked to antibodies for targeting of specific types of leukaemias.
APA, Harvard, Vancouver, ISO, and other styles
46

Webb, Steven D., Jonathan A. Sherratt, and Reginald G. Fish. "Cells behaving badly: a theoretical model for the Fas/FasL system in tumour immunology." Mathematical Biosciences 179, no. 2 (September 2002): 113–29. http://dx.doi.org/10.1016/s0025-5564(02)00120-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
47

De Weger, R. A., H. F. J. Dullens, R. J. De Boer, and W. Den Otter. "Mathematical analysis of the cellular immune reaction against tumour cells." Immunology Today 6, no. 11 (November 1985): 316–17. http://dx.doi.org/10.1016/0167-5699(85)90119-7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
48

Davern, Maria, Joanne Lysaght, Andrew Sheppard, Stephen Maher, Noel Donlon, John Reynolds, Fiona Connell, Conall Hayes, Ross King, and Anshul Bhardwaj. "776 A role for immune checkpoint blockade to enhance T cell-mediated responses in combination with chemotherapy in oesophageal adenocarcinoma." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (November 2020): A826—A827. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0776.

Full text
Abstract:
BackgroundCombining immune checkpoint inhibitors (ICIs) with immunogenic chemotherapies is a promising approach in oesophageal adenocarcinoma (OAC) to convert ‘cold’ tumours to ‘hot’ tumours expanding the efficacy of ICIs to a greater spectrum of patients.1 However, there is a vast array of immune checkpoints (ICs) expressed by T cells and the effect of ICIs in combination with chemotherapy regimens is largely unknown.2MethodsThe expression profile of a range of ICs on circulating and tumour-infiltrating T cells was assessed using flow cytometry prior to and post-neoadjuvant treatment and correlated with clinical parameters (n=20). PBMCs isolated from OAC blood were treated with single agent ICIs alone (single agent anti-PD-1, anti-PD-L1, anti-A2aR and anti-TIM-3 inhibition) and in combination with FLOT (5-Fluorouracil, oxaliplatin and docetaxel) and CROSS (carboplatin and paclitaxel) chemotherapy regimens. The production of anti-tumour cytokines by T cells was assessed in vitro by flow cytometry (n=6).ResultsIn the treatment-naïve and post-treatment setting, a range of ICs were expressed by circulating T cells and were significantly increased on tumour-infiltrating T cells, which included PD-L1, PD-L2, CD160, PD-1, CTLA-4, TIGIT, TIM-3, LAG-3, A2aR and ICOS (p<0.05) (figure 1). Pre-treatment circulating PD-1+ T cells positively correlated with pathological nodal status (p<0.05), (figure 2). Whereas tumour-infiltrating CD3+CTLA-4+ cells positively correlated with nodal metastasis and lymphovascular invasion (p<0.05). The percentage of tumour-infiltrating CD3+CTLA-4+ and CD3+ICOS+ cells was significantly lower post-neoadjuvant treatment (p<0.05) (figure 3). However, post-neoadjuvant treatment circulating CD3+PD-1+ cells and CD3+CD4+TIGIT+ cells positively correlated with a better treatment response, determined by PET/CT (p<0.05), (figure 4). ICIs enhanced T cell production of anti-tumour cytokines IL-2 and IFN-y alone and in combination with chemotherapy in vitro from treatment-naïve OAC patients (p<0.05).Abstract 776 Figure 1The percentage of T cells expressing PD-1 was significantly increased in tumour tissue compared with peripheral blood circulation in the treatment-naïve setting of OAC patients CD3+, CD3+ CD4+ and CD3+ CD8+ cells were screened for the surface expression of PD-1 in OAC patient blood pre-treatment blood and tumour tissue (n=20). Mann Whitney test **<0.001.Abstract 776 Figure 2Pre-treatment circulating PD-1+ T cells positively correlated with pathological nodal status and tumour-infiltrating CD3+CTLA-4+ cells positively correlated with nodal metastasis and lymphovascular invasion. The percentage of CD3+, CD3+CD4+ and CD3+CD8+ cells expressing ICs in peripheral circulation and infiltrating OAC tissue in the treatment-naïve setting was correlated with each other, patient demographics and clinical features of the tumour. Patient demographics and clinical features included gender (female=0, male=1), age, tumour type (OAC=0 and OGJ=1), neo-adjuvant treatment received (CROSS=0 and FLOT=1), treatment response (determined by radiographic features using PET/CT), tumour regression grade (TRG), clinical tumour stage and nodal involvement, pathological tumour stage and nodal involvement, body mass index (BMI kg/m2), peri-neural invasion, serosal invasion and lymph-vascular invasion. BMI and weight measurement was recorded post-treatment. Spearman correlation. Only significant data shown.Abstract 776 Figure 3The percentage of tumour-infiltrating T cells expressing CTLA-4 and ICOS were significantly lower post-neoadjuvant therapy in OAC tumour tissue. CD3+, CD3+ CD4+ and CD3+ CD8+ cells were screened for the surface expression of CTLA-4 and ICOS infiltrating OAC tissue pre-treatment and post-treatment (n=20). Mann Whitney test *<0.001.Abstract 776 Figure 4The percentage of circulating CD3+PD-1+ cells and CD3+CD4+TIGIT+ cells positively correlated with a better treatment response in the post-treatment setting. The percentage of CD3+, CD3+CD4+ and CD3+CD8+ cells expressing ICs in peripheral circulation and infiltrating OAC tissue in the post-neoadjuvant treatment setting was correlated with each other, patient demographics and clinical features of the tumour. Patient demographics and clinical features included gender (female=0, male=1), age, tumour type (OAC=0 and OGJ=1), neo-adjuvant treatment received (CROSS=0 and FLOT=1), treatment response (determined by radiographic features using PET/CT), tumour regression grade (TRG), clinical tumour stage and nodal involvement, pathological tumour stage and nodal involvement, body mass index (BMI kg/m2), peri-neural invasion, serosal invasion and lymph-vascular invasion. BMI and weight measurement was recorded post-treatment. Spearman correlation. Only significant data shown.ConclusionsT cells expressing ICs in circulation and infiltrating OAC tissue were adverse prognostic markers in the pre-treatment setting, perhaps due to their role in enabling tumour immune evasion and subsequent tumour progression. In contrast, T cells expressing ICs post-chemotherapy treatment in peripheral circulation were favorable prognostic markers. ICs are typically expressed by ‘hot’ tumours2 therefore, the presence of ICs in the post-treatment setting may be as a result of an induced-anti-tumour immune response following immunogenic chemotherapy/chemoradiotherapy treatment and may be a useful strategy for stratifying patients into chemotherapy/chemoradiotherapy responders or non-responders. A therapeutic rationale is also highlighted for combining ICIs with chemotherapy regimens in OAC patients to enhance anti-tumour T cell-mediated responses and potentially boost response rates to chemotherapy treatment.AcknowledgementsWe would like to thank all the patients who kindly donated their samples to our researchEthics ApprovalThe work was performed in accordance with the Code of Ethics of the World Medical Association (Declaration of Helsinki) for experiments involving human samples.ConsentPatients provided informed consent for sample and data acquisition, and the study received full ethical approval from the St. James’s Hospital/AMNCH Ethical Review Board.ReferencesDavern M, Lysaght J. Cooperation between chemotherapy and immunotherapy in gastroesophageal cancers. Cancer Lett 2020. https://doi.org/10.1016/j.canlet.2020.09.014Emens LA, Middleton G. The interplay of immunotherapy and chemotherapy: harnessing potential synergies. Cancer Immunol Res 2015;3:436–443.
APA, Harvard, Vancouver, ISO, and other styles
49

Martinez-Usatorre, A., E. Kadioglu, C. Cianciaruso, B. Torchia, J. Faget, E. Meylan, M. Schmittnaegel, I. Keklikoglou, and M. De Palma. "O4 Mechanisms of lung cancer hyper-progression promoted by PD-1 immune checkpoint blockade." Journal for ImmunoTherapy of Cancer 8, Suppl 2 (October 2020): A5.1—A5. http://dx.doi.org/10.1136/jitc-2020-itoc7.9.

Full text
Abstract:
BackgroundImmune checkpoint blockade (ICB) with antibodies against PD-1 or PD-L1 may provide therapeutic benefits in patients with non-small cell lung cancer (NSCLC). However, most tumours are resistant and cases of disease hyper-progression have also been reported.Materials and MethodsGenetically engineered mouse models of KrasG12Dp53null NSCLC were treated with cisplatin along with antibodies against angiopoietin-2/VEGFA, PD-1 and CSF1R. Tumour growth was monitored by micro-computed tomography and the tumour vasculature and immune cell infiltrates were assessed by immunofluorescence staining and flow cytometry.ResultsCombined angiopoietin-2/VEGFA blockade by a bispecific antibody (A2V) modulated the vasculature and abated immunosuppressive macrophages while increasing CD8+effector T cells in the tumours, achieving disease stabilization comparable or superior to cisplatin-based chemotherapy. However, these immunological responses were unexpectedly limited by the addition of a PD-1 antibody, which paradoxically enhanced progression of a fraction of the tumours through a mechanism involving regulatory T cells and macrophages. Elimination of tumour-associated macrophages with a CSF1R-blocking antibody induced NSCLC regression in combination with PD-1 blockade and cisplatin.ConclusionsThe immune cell composition of the tumour determines the outcome of PD-1 blockade. In NSCLC, high infiltration of regulatory T cells and immunosuppressive macrophages may account for tumour hyper-progression upon ICB.Disclosure InformationA. Martinez-Usatorre: None. E. Kadioglu: None. C. Cianciaruso: None. B. Torchia: None. J. Faget: None. E. Meylan: None. M. Schmittnaegel: None. I. Keklikoglou: None. M. De Palma: None.
APA, Harvard, Vancouver, ISO, and other styles
50

Cendrowicz, E., LJ Jacob, S. Greenwald, G. Huls, M. Dranitzki-Elhalel, Y. Pereg, A. Chajut, and E. Bremer. "P01.09 Dual signalling protein 107 triggers innate and adaptive immune response towards tumour cells." Journal for ImmunoTherapy of Cancer 8, Suppl 2 (October 2020): A12—A13. http://dx.doi.org/10.1136/jitc-2020-itoc7.22.

Full text
Abstract:
BackgroundDual signalling protein 107 (DSP107) is a trimeric fusion protein consisting of the extracellular domains of human SIRPα and 4-1BBL. SIRPα binds to CD47, frequently overexpressed on cancer cells, and 41BBL binds to 41BB on activated T-cells. The SIRPα domain triggers the innate immune response by inhibiting the CD47/SIRPα ‘don’t eat me’ signalling. It thus promotes phagocytosis of cancer cells by granulocytes, macrophages and dendritic cells. With its other side, 41BBL domain binds to pre-activated T cells and stimulates their expansion, cytokine production and cytolytic effector function. Our hypothesis is that augmented phagocytosis and improved co-localization of immune cells will lead to better antigen presentation towards activated T and B cells and the generation of memory T and B cells will be enforced. As result DSP107 might lead to immunity after rechallenge with the same tumour type.Materials and MethodsPrimary phagocytes were incubated with stained tumour cells in presence or absence of DSP107 or/and therapeutic antibodies. Fluorescence microscopy measured uptake of tumour cells by macrophages. FACS identified primary granulocytes positive for CD11b staining and membrane dye. HT1080-41BB cells were mixed with HT1080-CD47 or HT1080-wt in presence of DSP107 and IL-8 release to supernatant was measured by ELISA. Further, primary T cells were co-cultured with αCD3Fc and fluorescent protein transduced carcinoma cells at different DSP107 concentrations.ResultsThe number of granulocytes that phagocyte tumour cells was increased in presence of DSP107. Further, DSP107 not only stimulated more macrophages to engulf tumour cells, but also the number of tumour cells that were taken up per phagocyte rose. Already enhanced phagocytosis of tumour cells by therapeutic antibodies (e.g. Cetuximab, Rituximab and Trastuzumab) was improved even further by DSP107. A model system showed that activation of the 41BB/41BBL axis by DSP107 was dependent on cross-linking via CD47 domain. This indicates low off-target T cell activation. Apart from the model system, DSP107 stimulated primary T cells in co-culture with carcinoma cells (transduced to express αCD3 and a fluorescent protein). Cytolytic activity against carcinoma cells was improved and outgrowth of tumour cells was reduced in a dose dependant manner.ConclusionsDSP107 blocks the CD47/SIRPα checkpoint resulting in enhanced tumour cell phagocytosis and stimulates the 41BB/41BBL axis leading to T cell mediated tumour cell killing. DSP107 is a novel bifunctional therapeutic that targets and activates both innate and adaptive anticancer immune responses. DSP107 is a first-in-class drug candidate that can be used as a monotherapy or in combination with tumor-targeting monoclonal antibodies to trigger induction of anti-cancer immunity. DSP107 is currently tested in IND-enabling studies and clinical development is planned to commence in 2020.Disclosure InformationE. Cendrowicz: None. L.J. Jacob: A. Employment (full or part-time); Significant; KAHR Medical. S. Greenwald: A. Employment (full or part-time); Significant; KAHR Medical. G. Huls: None. M. Dranitzki-Elhalel: None. Y. Pereg: A. Employment (full or part-time); Significant; KAHR Medical. A. Chajut: A. Employment (full or part-time); Significant; KAHR Medical. E. Bremer: None.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the bibliographies on the topic 'Immunology; Tumour cells' for other source types:
Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography