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Journal articles on the topic 'Immuno evasione'

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Published: 9 March 2023
Last updated: 10 March 2023

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1

Baldwin, Louise A., Nenad Bartonicek, Jessica Yang, Sunny Z. Wu, Niantao Deng, Daniel Roden, Chia-Ling Chan, et al. "Abstract P1-04-04: Dna barcoding reveals ongoing immunoediting of clonal cancer populations during metastatic progression and in response to immunotherapy." Cancer Research 82, no. 4_Supplement (February 15, 2022): P1–04–04—P1–04–04. http://dx.doi.org/10.1158/1538-7445.sabcs21-p1-04-04.

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Abstract As cancers develop and spread they must continually evade immune destruction. Understanding mechanisms of immune evasion in cancer is clinically significant as demonstrated with the successes of immune checkpoint inhibitors. Breast cancer is known to be highly immune evasive and responds poorly to the current immunotherapies, indicating alternative immune pathways must be targeted. We hypothesise that there are unidentified genetic mechanisms that enable immune evasion in breast cancer. We aim to uncover and target these mechanisms to sensitise immune evasive breast cancer cells to immune destruction in the context of immunotherapy treatment. DNA barcoding technology offers a new approach to understanding immune evasion. By stably integrating a unique DNA barcode sequence into each cell, we can study clonal immune evasion in vivo. Using this technology, we identified cancer cell clones from the 4T1 murine mammary carcinoma cell line that are highly enriched in lung metastases following treatment with combination immunotherapy (anti-CTLA-4 plus anti-PD-1). We isolated these specific immune evasive clones and established them as clonal cell lines. We have identified stark clonal differences in both PD-L1 and MHC I expression at both the RNA and protein level, and shown that MHC I expression is only partially controlled by epigenetic mechanisms. In addition, immune evasive subclones co-cultured with stimulated T cells resulted in less activated T cells than their less evasive counterparts. Furthermore, RNA sequencing of these clones has identified a gene signature that is strongly associated with decreased survival in both the METABRIC and TCGA cohorts. We have demonstrated ongoing immunoediting in the 4T1 model in vivo, both during metastasis and immunotherapy treatment. We have also identified subclonal populations of cells within a single tumour utilising different mechanisms of immune evasion. RNA sequencing has revealed a gene signature strongly associated with poor survival of basal-like breast cancer in two cohorts. Further pathway-level analysis of the resulting gene signature is required to elucidate the drivers of this aggressive and immune evasive phenotype. By targeting newly identified mechanisms of immune evasion in combination with current immunotherapies, we hope to improve the long-term survival of breast cancer patients. Citation Format: Louise A Baldwin, Nenad Bartonicek, Jessica Yang, Sunny Z Wu, Niantao Deng, Daniel Roden, Chia-Ling Chan, Ghamdan Al-Eryani, Damien J Zanker, Belinda S Parker, Alexander Swarbrick, Simon Junankar. Dna barcoding reveals ongoing immunoediting of clonal cancer populations during metastatic progression and in response to immunotherapy [abstract]. In: Proceedings of the 2021 San Antonio Breast Cancer Symposium; 2021 Dec 7-10; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2022;82(4 Suppl):Abstract nr P1-04-04.
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2

Lehnert, Teresa, Maria T. E. Prauße, Kerstin Hünniger, Jan-Philipp Praetorius, Oliver Kurzai, and Marc Thilo Figge. "Comparative assessment of immune evasion mechanisms in human whole-blood infection assays by a systems biology approach." PLOS ONE 16, no. 4 (April 1, 2021): e0249372. http://dx.doi.org/10.1371/journal.pone.0249372.

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Computer simulations of mathematical models open up the possibility of assessing hypotheses generated by experiments on pathogen immune evasion in human whole-blood infection assays. We apply an interdisciplinary systems biology approach in which virtual infection models implemented for the dissection of specific immune mechanisms are combined with experimental studies to validate or falsify the respective hypotheses. Focusing on the assessment of mechanisms that enable pathogens to evade the immune response in the early time course of a whole-blood infection, the least-square error (LSE) as a measure for the quantitative agreement between the theoretical and experimental kinetics is combined with the Akaike information criterion (AIC) as a measure for the model quality depending on its complexity. In particular, we compare mathematical models with three different types of pathogen immune evasion as well as all their combinations: (i) spontaneous immune evasion, (ii) evasion mediated by immune cells, and (iii) pre-existence of an immune-evasive pathogen subpopulation. For example, by testing theoretical predictions in subsequent imaging experiments, we demonstrate that the simple hypothesis of having a subpopulation of pre-existing immune-evasive pathogens can be ruled out. Furthermore, in this study we extend our previous whole-blood infection assays for the two fungal pathogens Candida albicans and C. glabrata by the bacterial pathogen Staphylococcus aureus and calibrated the model predictions to the time-resolved experimental data for each pathogen. Our quantitative assessment generally reveals that models with a lower number of parameters are not only scored with better AIC values, but also exhibit lower values for the LSE. Furthermore, we describe in detail model-specific and pathogen-specific patterns in the kinetics of cell populations that may be measured in future experiments to distinguish and pinpoint the underlying immune mechanisms.
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3

Zindl, C. L., and D. D. Chaplin. "Tumor Immune Evasion." Science 328, no. 5979 (May 6, 2010): 697–98. http://dx.doi.org/10.1126/science.1190310.

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4

Seton-Rogers, Sarah. "Driving immune evasion." Nature Reviews Cancer 18, no. 2 (January 25, 2018): 67. http://dx.doi.org/10.1038/nrc.2018.5.

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5

Mueller, K. L. "Immune Evasion Tactic." Science Signaling 4, no. 157 (January 25, 2011): ec27-ec27. http://dx.doi.org/10.1126/scisignal.4157ec27.

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6

Mascola, John R. "Engineering immune evasion." Nature 441, no. 7090 (May 2006): 161. http://dx.doi.org/10.1038/441161a.

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7

Fehervari, Zoltan. "Glioma immune evasion." Nature Immunology 18, no. 5 (May 2017): 487. http://dx.doi.org/10.1038/ni.3736.

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8

Fitzpatrick, David R., and Helle Bielefeldt-Ohmann. "Mechanisms of herpesvirus immuno-evasion." Microbial Pathogenesis 10, no. 4 (April 1991): 253–59. http://dx.doi.org/10.1016/0882-4010(91)90009-y.

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9

Upadhyay, Ranjan, Linda Hammerich, Paul Peng, Brian Brown, Miriam Merad, and Joshua Brody. "Lymphoma: Immune Evasion Strategies." Cancers 7, no. 2 (April 30, 2015): 736–62. http://dx.doi.org/10.3390/cancers7020736.

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10

Tsukerman, Pinchas, Jonatan Enk, and Ofer Mandelboim. "Metastamir-mediated immune evasion." OncoImmunology 2, no. 1 (January 2013): e22245. http://dx.doi.org/10.4161/onci.22245.

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11

Ramanan, Parameshwaran, Reed S. Shabman, Craig S. Brown, Gaya K. Amarasinghe, Christopher F. Basler, and Daisy W. Leung. "Filoviral Immune Evasion Mechanisms." Viruses 3, no. 9 (September 7, 2011): 1634–49. http://dx.doi.org/10.3390/v3091634.

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12

Foster, Timothy J. "Immune evasion by staphylococci." Nature Reviews Microbiology 3, no. 12 (December 2005): 948–58. http://dx.doi.org/10.1038/nrmicro1289.

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13

David, Rachel. "Immune evasion through silence." Nature Reviews Microbiology 11, no. 8 (July 16, 2013): 509. http://dx.doi.org/10.1038/nrmicro3084.

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14

Smith, Geoffrey L., Julian A. Symons, Anu Khanna, Alain Vanderplasschen, and Antonio Alcami. "Vaccinia virus immune evasion." Immunological Reviews 159, no. 1 (October 1997): 137–54. http://dx.doi.org/10.1111/j.1600-065x.1997.tb01012.x.

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15

Mahr, Jeffrey A., and Linda R. Gooding. "Immune evasion by adenoviruses." Immunological Reviews 168, no. 1 (April 1999): 121–30. http://dx.doi.org/10.1111/j.1600-065x.1999.tb01287.x.

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16

KINIWA, Yukiko. "Immune-evasion of melanoma." Skin Cancer 24, no. 2 (2009): 159–63. http://dx.doi.org/10.5227/skincancer.24.159.

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17

Mueller, K. L. "Cytomegalovirus Immune Evasion Strategy." Science Signaling 3, no. 116 (April 6, 2010): ec103-ec103. http://dx.doi.org/10.1126/scisignal.3116ec103.

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18

Blacklaws, Barbara. "Immune evasion by HSV." Trends in Microbiology 6, no. 9 (September 1998): 352. http://dx.doi.org/10.1016/s0966-842x(98)01334-1.

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19

Rooijakkers, Suzan H. M., Kok P. M. van Kessel, and Jos A. G. van Strijp. "Staphylococcal innate immune evasion." Trends in Microbiology 13, no. 12 (December 2005): 596–601. http://dx.doi.org/10.1016/j.tim.2005.10.002.

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20

Smith, Geoffrey L. "Vaccinia virus immune evasion." Immunology Letters 65, no. 1-2 (January 1999): 55–62. http://dx.doi.org/10.1016/s0165-2478(98)00125-4.

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21

Damian, R. T., and J. K. Dineen. "Workshop 1E: Immune evasion." International Journal for Parasitology 17, no. 5 (July 1987): 1005–6. http://dx.doi.org/10.1016/0020-7519(87)90198-6.

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22

McFadden, Grant, and Steven H. Nazarian. "Immune evasion by poxviruses." Future Virology 1, no. 1 (January 2006): 123–32. http://dx.doi.org/10.2217/17460794.1.1.123.

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23

Buckland, Jenny. "Immune evasion by anthrax." Nature Reviews Immunology 2, no. 11 (November 2002): 810. http://dx.doi.org/10.1038/nri942.

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24

Cabrita, Rita, Shamik Mitra, Adriana Sanna, Henrik Ekedahl, Kristina Lövgren, Håkan Olsson, Christian Ingvar, et al. "The Role of PTEN Loss in Immune Escape, Melanoma Prognosis and Therapy Response." Cancers 12, no. 3 (March 21, 2020): 742. http://dx.doi.org/10.3390/cancers12030742.

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Checkpoint blockade therapies have changed the clinical management of metastatic melanoma patients considerably, showing survival benefits. Despite the clinical success, not all patients respond to treatment or they develop resistance. Although there are several treatment predictive biomarkers, understanding therapy resistance and the mechanisms of tumor immune evasion is crucial to increase the frequency of patients benefiting from treatment. The PTEN gene is thought to promote immune evasion and is frequently mutated in cancer and melanoma. Another feature of melanoma tumors that may affect the capacity of escaping T-cell recognition is melanoma cell dedifferentiation characterized by decreased expression of the microphtalmia-associated transcription factor (MITF) gene. In this study, we have explored the role of PTEN in prognosis, therapy response, and immune escape in the context of MITF expression using immunostaining and genomic data from a large cohort of metastatic melanoma. We confirmed in our cohort that PTEN alterations promote immune evasion highlighted by decreased frequency of T-cell infiltration in such tumors, resulting in a worse patient survival. More importantly, our results suggest that dedifferentiated PTEN negative melanoma tumors have poor patient outcome, no T-cell infiltration, and transcriptional properties rendering them resistant to targeted- and immuno-therapy.
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25

Ravindran, N. S., M. Mohamed Sheriff, and P. Krishnapriya. "Analysis of tumour-immune evasion with chemo-immuno therapeutic treatment with quadratic optimal control." Journal of Biological Dynamics 11, no. 1 (January 2017): 480–503. http://dx.doi.org/10.1080/17513758.2017.1381280.

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26

Mancini, Mathieu, and Silvia M. Vidal. "Mechanisms of Natural Killer Cell Evasion Through Viral Adaptation." Annual Review of Immunology 38, no. 1 (April 26, 2020): 511–39. http://dx.doi.org/10.1146/annurev-immunol-082619-124440.

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The continuous interactions between host and pathogens during their coevolution have shaped both the immune system and the countermeasures used by pathogens. Natural killer (NK) cells are innate lymphocytes that are considered central players in the antiviral response. Not only do they express a variety of inhibitory and activating receptors to discriminate and eliminate target cells but they can also produce immunoregulatory cytokines to alert the immune system. Reciprocally, several unrelated viruses including cytomegalovirus, human immunodeficiency virus, influenza virus, and dengue virus have evolved a multitude of mechanisms to evade NK cell function, such as the targeting of pathways for NK cell receptors and their ligands, apoptosis, and cytokine-mediated signaling. The studies discussed in this article provide further insights into the antiviral function of NK cells and the pathways involved, their constituent proteins, and ways in which they could be manipulated for host benefit.
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27

Sharpe, Martyn A., David S. Baskin, Amanda V. Jenson, and Alexandra M. Baskin. "Hijacking Sexual Immuno-Privilege in GBM—An Immuno-Evasion Strategy." International Journal of Molecular Sciences 22, no. 20 (October 12, 2021): 10983. http://dx.doi.org/10.3390/ijms222010983.

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Regulatory T-cells (Tregs) are immunosuppressive T-cells, which arrest immune responses to ‘Self’ tissues. Some immunosuppressive Tregs that recognize seminal epitopes suppress immune responses to the proteins in semen, in both men and women. We postulated that GBMs express reproductive-associated proteins to manipulate reproductive Tregs and to gain immune privilege. We analyzed four GBM transcriptome databases representing ≈900 tumors for hypoxia-responsive Tregs, steroidogenic pathways, and sperm/testicular and placenta-specific genes, stratifying tumors by expression. In silico analysis suggested that the presence of reproductive-associated Tregs in GBM tumors was associated with worse patient outcomes. These tumors have an androgenic signature, express male-specific antigens, and attract reproductive-associated Related Orphan Receptor C (RORC)-Treg immunosuppressive cells. GBM patient sera were interrogated for the presence of anti-sperm/testicular antibodies, along with age-matched controls, utilizing monkey testicle sections. GBM patient serum contained anti-sperm/testicular antibodies at levels > six-fold that of controls. Myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs) are associated with estrogenic tumors which appear to mimic placental tissue. We demonstrate that RORC-Tregs drive poor patient outcome, and Treg infiltration correlates strongly with androgen levels. Androgens support GBM expression of sperm/testicular proteins allowing Tregs from the patient’s reproductive system to infiltrate the tumor. In contrast, estrogen appears responsible for MDSC/TAM immunosuppression.
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28

Denisov, Stepan S., Mercedes Ramírez-Escudero, Alexandra C. A. Heinzmann, Johannes H. Ippel, Philip E. Dawson, Rory R. Koenen, Tilman M. Hackeng, Bert J. C. Janssen, and Ingrid Dijkgraaf. "Structural characterization of anti-CCL5 activity of the tick salivary protein evasin-4." Journal of Biological Chemistry 295, no. 42 (August 14, 2020): 14367–78. http://dx.doi.org/10.1074/jbc.ra120.013891.

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Ticks, as blood-sucking parasites, have developed a complex strategy to evade and suppress host immune responses during feeding. The crucial part of this strategy is expression of a broad family of salivary proteins, called Evasins, to neutralize chemokines responsible for cell trafficking and recruitment. However, structural information about Evasins is still scarce, and little is known about the structural determinants of their binding mechanism to chemokines. Here, we studied the structurally uncharacterized Evasin-4, which neutralizes a broad range of CC-motif chemokines, including the chemokine CC-motif ligand 5 (CCL5) involved in atherogenesis. Crystal structures of Evasin-4 and E66S CCL5, an obligatory dimeric variant of CCL5, were determined to a resolution of 1.3–1.8 Å. The Evasin-4 crystal structure revealed an L-shaped architecture formed by an N- and C-terminal subdomain consisting of eight β-strands and an α-helix that adopts a substantially different position compared with closely related Evasin-1. Further investigation into E66S CCL5–Evasin-4 complex formation with NMR spectroscopy showed that residues of the N terminus are involved in binding to CCL5. The peptide derived from the N-terminal region of Evasin-4 possessed nanomolar affinity to CCL5 and inhibited CCL5 activity in monocyte migration assays. This suggests that Evasin-4 derivatives could be used as a starting point for the development of anti-inflammatory drugs.
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29

Wilson, Emily C., Yinshen Wee, Junhua Wang, Coulson P. Rich, Aaron Rogers, Roger K. Wolff, Sheri L. Holmen, and Allie H. Grossmann. "Abstract B50: Discovery of multiple mechanisms of immune evasion that accelerate primary melanomagenesis in a genetic model with low tumor mutation burden." Cancer Immunology Research 10, no. 12_Supplement (December 1, 2022): B50. http://dx.doi.org/10.1158/2326-6074.tumimm22-b50.

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Abstract Although immune checkpoint blockade (ICB) therapy can improve outcomes in advanced melanoma, early detection and treatment focused on preventing metastasis remain the optimal approaches for superior survival. Immune evasion occurs early in melanoma development and as such, some patients with high-risk Stage II (nonmetastatic) disease benefit from ICB. These human data highlight a critical need to understand the complex process of immune evasion during melanoma formation and early progression. To this end, we interrogated the tumor immune microenvironment of the RCAS-CRE inducible, Dct::TVA; BrafV600E; Cdkn2aNull murine model of melanoma. Tumor development occurs rapidly and at high frequency in these mice, without exposure to ultraviolet light or mutagenic carcinogens, modeling an important molecular class of melanoma with low mutation burden, which generally occurs in young patients. Using single-cell RNA sequencing and immunostaining, we discovered that primary tumors show evidence of an adaptive immune response that is restricted by myeloid-derived suppressor cells, regulatory T cells and PD-L1 expression. Systemic anti-PD-1 treatment reduced tumor incidence and significantly delayed tumor onset. Despite the low mutation burden, our data demonstrate the presence of a smoldering adaptive immune response that can be unleashed with ICB to limit tumor formation. Importantly, unlike syngeneic allograft models, our genetic model provides a unique opportunity to interrogate tumor-intrinsic mechanisms of immune evasion during an auspicious time window that spans from - tumor initiation to high-risk, pre-metastatic disease. Thus, we have identified a useful in vivo tool for the discovery of novel mechanisms of immune evasion and for testing therapeutic interventions in early-stage disease. Citation Format: Emily C Wilson, Yinshen Wee, Junhua Wang, Coulson P Rich, Aaron Rogers, Roger K Wolff, Sheri L Holmen, Allie H Grossmann. Discovery of multiple mechanisms of immune evasion that accelerate primary melanomagenesis in a genetic model with low tumor mutation burden [abstract]. In: Proceedings of the AACR Special Conference: Tumor Immunology and Immunotherapy; 2022 Oct 21-24; Boston, MA. Philadelphia (PA): AACR; Cancer Immunol Res 2022;10(12 Suppl):Abstract nr B50.
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30

Zugazagoitia, Jon, Sonia Molina-Pinelo, Fernando Lopez-Rios, and Luis Paz-Ares. "Biological therapies in nonsmall cell lung cancer." European Respiratory Journal 49, no. 3 (March 2017): 1601520. http://dx.doi.org/10.1183/13993003.01520-2016.

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Biological therapies have improved survival outcomes of advanced-stage nonsmall cell lung cancer (NSCLC). Genotype-directed therapies have changed treatment paradigms of patients withEGFR-mutant andALK/ROS1-rearranged lung adenocarcinomas, and the list of druggable targets with demonstrated clinical actionability (BRAF, MET, RET, NTRK1andHER2) continues to expand. Furthermore, we have incrementally understood the mechanisms of cancer immune evasion and foresee ways to effectively circumvent them, particularly at the immune checkpoint level. Drugs targeting the tumour immune-evasive PD-1 pathway have demonstrated remarkable treatment benefits in this disease, with a non-negligible fraction of patients potentially receiving long-term survival benefits. Herein, we briefly discuss the role of various medical disciplines in the management of advanced-stage NSCLC and review the most relevant biological therapies for this disease, with particular emphasis in genotype-directed therapies and immune checkpoint inhibitors.
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31

Seliger, Barbara. "Strategies of Tumor Immune Evasion." BioDrugs 19, no. 6 (2005): 347–54. http://dx.doi.org/10.2165/00063030-200519060-00002.

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32

SHIMADA, Takahiro, and Itaru MATSUMURA. "Immune evasion of Pseudomonas aeruginosa." Japanese Journal of Clinical Immunology 37, no. 1 (2014): 33–41. http://dx.doi.org/10.2177/jsci.37.33.

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33

Askar, Hussam, Shengli Chen, Huafang Hao, Xinmin Yan, Lina Ma, Yongsheng Liu, and Yuefeng Chu. "Immune Evasion of Mycoplasma bovis." Pathogens 10, no. 3 (March 4, 2021): 297. http://dx.doi.org/10.3390/pathogens10030297.

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Mycoplasma bovis (M. bovis) causes various chronic inflammatory diseases, including mastitis and bronchopneumonia, in dairy and feed cattle. It has been found to suppress the host immune response during infection, leading to the development of chronic conditions. Both in vitro and in vivo studies have confirmed that M. bovis can induce proinflammatory cytokines and chemokines in the host. This consists of an inflammatory response in the host that causes pathological immune damage, which is essential for the pathogenic mechanism of M. bovis. Additionally, M. bovis can escape host immune system elimination and, thus, cause chronic infection. This is accomplished by preventing phagocytosis and inhibiting key responses, including the neutrophil respiratory burst and the development of nitric oxide (NO) and inducible nitric oxide synthase (iNOS) that lead to the creation of an extracellular bactericidal network, in addition to inhibiting monocyte and alveolar macrophage apoptosis and inducing monocytes to produce anti-inflammatory factors, thus inducing the apoptosis of peripheral blood mononuclear cells (PBMCs), inhibiting their proliferative response and resulting in their invasion. Together, these conditions lead to long-term M. bovis infection. In terms of the pathogenic mechanism, M. bovis may invade specific T-cell subsets and induce host generation of exhausted T-cells, which helps it to escape immune clearance. Moreover, the M. bovis antigen exhibits high-frequency variation in size and expression period, which allows it to avoid activation of the host humoral immune response. This review includes some recent advances in studying the immune response to M. bovis. These may help to further understand the host immune response against M. bovis and to develop potential therapeutic approaches to control M. bovis infection.
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34

Eddy, Kevinn, and Suzie Chen. "Overcoming Immune Evasion in Melanoma." International Journal of Molecular Sciences 21, no. 23 (November 26, 2020): 8984. http://dx.doi.org/10.3390/ijms21238984.

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Melanoma is the most aggressive and dangerous form of skin cancer that develops from transformed melanocytes. It is crucial to identify melanoma at its early stages, in situ, as it is “curable” at this stage. However, after metastasis, it is difficult to treat and the five-year survival is only 25%. In recent years, a better understanding of the etiology of melanoma and its progression has made it possible for the development of targeted therapeutics, such as vemurafenib and immunotherapies, to treat advanced melanomas. In this review, we focus on the molecular mechanisms that mediate melanoma development and progression, with a special focus on the immune evasion strategies utilized by melanomas, to evade host immune surveillances. The proposed mechanism of action and the roles of immunotherapeutic agents, ipilimumab, nivolumab, pembrolizumab, and atezolizumab, adoptive T- cell therapy plus T-VEC in the treatment of advanced melanoma are discussed. In this review, we implore that a better understanding of the steps that mediate melanoma onset and progression, immune evasion strategies exploited by these tumor cells, and the identification of biomarkers to predict treatment response are critical in the design of improved strategies to improve clinical outcomes for patients with this deadly disease.
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35

Sykes, Megan. "Immune Evasion by Chimeric Trachea." New England Journal of Medicine 362, no. 2 (January 14, 2010): 172–74. http://dx.doi.org/10.1056/nejme0908366.

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36

Abendroth, Allison, and Ann Arvin. "Varicella-zoster virus immune evasion." Immunological Reviews 168, no. 1 (April 1999): 143–56. http://dx.doi.org/10.1111/j.1600-065x.1999.tb01289.x.

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37

Ferrarelli, Leslie K. "FAK directs tumor immune evasion." Science 358, no. 6368 (December 7, 2017): 1266.5–1267. http://dx.doi.org/10.1126/science.358.6368.1266-e.

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38

Nagata, Shigekazu. "Fas ligand and immune evasion." Nature Medicine 2, no. 12 (December 1996): 1306–7. http://dx.doi.org/10.1038/nm1296-1306.

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39

Audet, Jonathan, and Gary P. Kobinger. "Immune Evasion in Ebolavirus Infections." Viral Immunology 28, no. 1 (February 2015): 10–18. http://dx.doi.org/10.1089/vim.2014.0066.

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40

Bradbury, Jane. "Malarial immune evasion mechanism uncovered." Lancet Infectious Diseases 5, no. 6 (June 2005): 335. http://dx.doi.org/10.1016/s1473-3099(05)70130-4.

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41

Flávia Nardy, Ana, Célio Geraldo Freire-de-Lima, and Alexandre Morrot. "Immune Evasion Strategies ofTrypanosoma cruzi." Journal of Immunology Research 2015 (2015): 1–7. http://dx.doi.org/10.1155/2015/178947.

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Microbes have evolved a diverse range of strategies to subvert the host immune system. The protozoan parasiteTrypanosoma cruzi, the causative agent of Chagas disease, provides a good example of such adaptations. This parasite targets a broad spectrum of host tissues including both peripheral and central lymphoid tissues. Rapid colonization of the host gives rise to a systemic acute response which the parasite must overcome. The parasite in fact undermines both innate and adaptive immunity. It interferes with the antigen presenting function of dendritic cells via an action on host sialic acid-binding Ig-like lectin receptors. These receptors also induce suppression of CD4+T cells responses, and we presented evidence that the sialylation of parasite-derived mucins is required for the inhibitory effects on CD4 T cells. In this review we highlight the major mechanisms used byTrypanosoma cruzito overcome host immunity and discuss the role of parasite colonization of the central thymic lymphoid tissue in chronic disease.
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42

Alcami, Antonio, and Ulrich H. Koszinowski. "Viral mechanisms of immune evasion." Trends in Microbiology 8, no. 9 (September 2000): 410–18. http://dx.doi.org/10.1016/s0966-842x(00)01830-8.

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43

Alcami, Antonio, and Ulrich H. Koszinowski. "Viral mechanisms of immune evasion." Immunology Today 21, no. 9 (September 2000): 447–55. http://dx.doi.org/10.1016/s0167-5699(00)01699-6.

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44

Dunlop, Lance R., Katherine A. Oehlberg, Jeremy J. Reid, Dilek Avci, and Ariella M. Rosengard. "Variola virus immune evasion proteins." Microbes and Infection 5, no. 11 (September 2003): 1049–56. http://dx.doi.org/10.1016/s1286-4579(03)00194-1.

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45

Basler, Christopher F. "Innate immune evasion by filoviruses." Virology 479-480 (May 2015): 122–30. http://dx.doi.org/10.1016/j.virol.2015.03.030.

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Ye, Jing, Bibo Zhu, Zhen F. Fu, Huanchun Chen, and Shengbo Cao. "Immune evasion strategies of flaviviruses." Vaccine 31, no. 3 (January 2013): 461–71. http://dx.doi.org/10.1016/j.vaccine.2012.11.015.

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Kuipery, Adrian, Adam J. Gehring, and Masanori Isogawa. "Mechanisms of HBV immune evasion." Antiviral Research 179 (July 2020): 104816. http://dx.doi.org/10.1016/j.antiviral.2020.104816.

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Alcami, Antonio, and Ulrich H. Koszinowski. "Viral mechanisms of immune evasion." Molecular Medicine Today 6, no. 9 (September 2000): 365–72. http://dx.doi.org/10.1016/s1357-4310(00)01775-5.

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Stevenson, Philip G. "Immune evasion by gamma-herpesviruses." Current Opinion in Immunology 16, no. 4 (August 2004): 456–62. http://dx.doi.org/10.1016/j.coi.2004.05.002.

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Sakar, Mahmut Selman. "Immune evasion by designer microrobots." Science Robotics 5, no. 43 (June 17, 2020): eabc7620. http://dx.doi.org/10.1126/scirobotics.abc7620.

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