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Journal articles on the topic 'Immune subversion'

Author: Grafiati

Published: 16 November 2024

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1

Melief, C. J. M., T. Braciale, U. Kozinowski, H. Hengartner, A. McMichael, R. Steinman, H. Morse, and A. Rickinson. "Subversion of immune responses." Research in Immunology 144, no. 6-7 (January 1993): 534–36. http://dx.doi.org/10.1016/0923-2494(93)80163-s.

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2

Baldari, Cosima T., Antonio Lanzavecchia, and John L. Telford. "Immune subversion by Helicobacter pylori." Trends in Immunology 26, no. 4 (April 2005): 199–207. http://dx.doi.org/10.1016/j.it.2005.01.007.

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3

Lachmann, P. J. "Microbial subversion of the immune response." Proceedings of the National Academy of Sciences 99, no. 13 (June 19, 2002): 8461–62. http://dx.doi.org/10.1073/pnas.132284499.

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4

Tortorella, Domenico, Benjamin E. Gewurz, Margo H. Furman, Danny J. Schust, and Hidde L. Ploegh. "Viral Subversion of the Immune System." Annual Review of Immunology 18, no. 1 (April 2000): 861–926. http://dx.doi.org/10.1146/annurev.immunol.18.1.861.

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5

Baxt, L. A., A. C. Garza-Mayers, and M. B. Goldberg. "Bacterial Subversion of Host Innate Immune Pathways." Science 340, no. 6133 (May 9, 2013): 697–701. http://dx.doi.org/10.1126/science.1235771.

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6

HARNETT, WILLIAM, and L. H. CHAPPELL. "Subversion of immune cell signalling by parasites." Parasitology 130, S1 (March 2005): S1—S2. http://dx.doi.org/10.1017/s0031182005008334.

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7

MAULE, A. G., T. A. DAY, and L. H. CHAPPELL. "Subversion of immune cell signalling by parasites." Parasitology 131, S1 (March 29, 2006): S1. http://dx.doi.org/10.1017/s0031182005009388.

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8

Marrack, Philippa, and John Kappler. "Subversion of the immune system by pathogens." Cell 76, no. 2 (January 1994): 323–32. http://dx.doi.org/10.1016/0092-8674(94)90339-5.

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9

Scott, Terence, and Louis Nel. "Subversion of the Immune Response by Rabies Virus." Viruses 8, no. 8 (August 19, 2016): 231. http://dx.doi.org/10.3390/v8080231.

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10

Buzoni-Gatel, Dominique, and Catherine Werts. "Toxoplasma gondii and subversion of the immune system." Trends in Parasitology 22, no. 10 (October 2006): 448–52. http://dx.doi.org/10.1016/j.pt.2006.08.002.

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11

HAIG, D. M. "Subversion and piracy: DNA viruses and immune evasion." Research in Veterinary Science 70, no. 3 (June 2001): 205–19. http://dx.doi.org/10.1053/rvsc.2001.0462.

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12

Lachmann, Peter J. "Microbial immunology: A new mechanism for immune subversion." Current Biology 8, no. 3 (January 1998): R99—R101. http://dx.doi.org/10.1016/s0960-9822(98)70057-0.

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13

Xiao, Tsan Sam. "Subversion of Innate Immune Signaling Through Molecular Mimicry." Journal of Clinical Immunology 30, no. 5 (June 30, 2010): 638–42. http://dx.doi.org/10.1007/s10875-010-9435-0.

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14

Acha-Orbea, Hans, and H. Robson MacDonald. "Subversion of host immune responses by viral superantigens." Trends in Microbiology 1, no. 1 (April 1993): 32–34. http://dx.doi.org/10.1016/0966-842x(93)90022-j.

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15

Hajishengallis, George. "Periodontitis: from microbial immune subversion to systemic inflammation." Nature Reviews Immunology 15, no. 1 (December 23, 2014): 30–44. http://dx.doi.org/10.1038/nri3785.

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16

Park, Hae-Young, Lalage M. Wakefield, and Mizuko Mamura. "Regulation of Tumor Immune Surveillance and Tumor Immune Subversion by TGF-β." Immune Network 9, no. 4 (2009): 122. http://dx.doi.org/10.4110/in.2009.9.4.122.

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17

Pontejo, Sergio M., Philip M. Murphy, and James E. Pease. "Chemokine Subversion by Human Herpesviruses." Journal of Innate Immunity 10, no. 5-6 (2018): 465–78. http://dx.doi.org/10.1159/000492161.

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Viruses use diverse molecular mechanisms to exploit and evade the immune response. Herpesviruses, in particular, encode functional chemokine and chemokine receptor homologs pirated from the host, as well as secreted chemokine-binding proteins with unique structures. Multiple functions have been described for herpesvirus chemokine components, including attraction of target cells, blockade of leukocyte migration, and modulation of gene expression and cell entry by the virus. Here we review current concepts about how human herpesvirus chemokines, chemokine receptors, and chemokine-binding proteins may be used to shape a proviral state in the host.

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18

Franco, Luis H., Stephen M. Beverley, and Dario S. Zamboni. "Innate Immune Activation and Subversion of Mammalian Functions byLeishmaniaLipophosphoglycan." Journal of Parasitology Research 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/165126.

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Leishmaniapromastigotes express several prominent glycoconjugates, either secreted or anchored to the parasite surface. Of these lipophosphoglycan (LPG) is the most abundant, and along with other phosphoglycan-bearing molecules, plays important roles in parasite infectivity and pathogenesis in both the sand fly and the mammalian host. Besides its contribution for parasite survival in the sand fly vector, LPG is important for modulation the host immune responses to favor the establishment of mammalian infection. This review will summarize the current knowledge regarding the role of LPG inLeishmaniainfectivity, focusing on the interaction of LPG and innate immune cells and in the subversion of mammalian functions by this molecule.

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19

Fernie-King, B., D. J. Seilly, A. Davies, and P. J. Lachmann. "Subversion of the innate immune response by micro-organisms." Annals of the Rheumatic Diseases 61, Supplement 2 (November 1, 2002): 8ii—12. http://dx.doi.org/10.1136/ard.61.suppl_2.ii8.

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20

Jude, Brooke A., Yelena Pobezinskaya, Jennifer Bishop, Susannah Parke, Ruslan M. Medzhitov, Alexander V. Chervonsky, and Tatyana V. Golovkina. "Subversion of the innate immune system by a retrovirus." Nature Immunology 4, no. 6 (May 5, 2003): 573–78. http://dx.doi.org/10.1038/ni926.

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21

Small, Sara, Yazan Numan, and Leonidas C. Platanias. "Innate Immune Mechanisms and Immunotherapy of Myeloid Malignancies." Biomedicines 9, no. 11 (November 6, 2021): 1631. http://dx.doi.org/10.3390/biomedicines9111631.

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Similar to other cancers, myeloid malignancies are thought to subvert the immune system during their development. This subversion occurs via both malignant cell-autonomous and non-autonomous mechanisms and involves manipulation of the innate and adaptive immune systems. Multiple strategies are being studied to rejuvenate, redirect, or re-enforce the immune system in order to fight off myeloid malignancies. So far, the most successful strategies include interferon treatment and antibody-based therapies, though chimeric antigen receptor (CAR) cells and immune checkpoint inhibitors are also promising therapies. In this review, we discuss the inherent immune mechanisms of defense against myeloid malignancies, currently-approved agents, and agents under investigation. Overall, we evaluate the efficacy and potential of immuno-oncology in the treatment of myeloid malignancies.

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22

Lo Cigno, Irene, Federica Calati, Silvia Albertini, and Marisa Gariglio. "Subversion of Host Innate Immunity by Human Papillomavirus Oncoproteins." Pathogens 9, no. 4 (April 17, 2020): 292. http://dx.doi.org/10.3390/pathogens9040292.

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The growth of human papillomavirus (HPV)-transformed cells depends on the ability of the viral oncoproteins E6 and E7, especially those from high-risk HPV16/18, to manipulate the signaling pathways involved in cell proliferation, cell death, and innate immunity. Emerging evidence indicates that E6/E7 inhibition reactivates the host innate immune response, reversing what until then was an unresponsive cellular state suitable for viral persistence and tumorigenesis. Given that the disruption of distinct mechanisms of immune evasion is an attractive strategy for cancer therapy, the race is on to gain a better understanding of E6/E7-induced immune escape and cancer progression. Here, we review recent literature on the interplay between E6/E7 and the innate immune signaling pathways cGAS/STING/TBK1, RIG-I/MAVS/TBK1, and Toll-like receptors (TLRs). The overall emerging picture is that E6 and E7 have evolved broad-spectrum mechanisms allowing for the simultaneous depletion of multiple rather than single innate immunity effectors. The cGAS/STING/TBK1 pathway appears to be the most heavily impacted, whereas the RIG-I/MAVS/TBK1, still partially functional in HPV-transformed cells, can be activated by the powerful RIG-I agonist M8, triggering the massive production of type I and III interferons (IFNs), which potentiates chemotherapy-mediated cell killing. Overall, the identification of novel therapeutic targets to restore the innate immune response in HPV-transformed cells could transform the way HPV-associated cancers are treated.

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23

Quaranta, Valeria, and Michael C. Schmid. "Macrophage-Mediated Subversion of Anti-Tumour Immunity." Cells 8, no. 7 (July 19, 2019): 747. http://dx.doi.org/10.3390/cells8070747.

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Despite the incredible clinical benefits obtained by the use of immune checkpoint blockers (ICBs), resistance is still common for many types of cancer. Central for ICBs to work is activation and infiltration of cytotoxic CD8+ T cells following tumour-antigen recognition. However, it is now accepted that even in the case of immunogenic tumours, the effector functions of CD8+ T cells are highly compromised by the presence of an immunosuppressive tumour microenvironment (TME) at the tumour site. Tumour-associated macrophages (TAMs) are among the most abundant non-malignant stromal cell types within the TME and they are crucial drivers of tumour progression, metastasis and resistance to therapy. TAMs are able to regulate either directly or indirectly various aspects of tumour immunity, including T cell recruitment and functions. In this review we discuss the mechanisms by which TAMs subvert CD8+ T cell immune surveillance and how their targeting in combination with ICBs represents a very powerful therapeutic strategy.

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24

Riebisch, Anna Katharina, and Sabrina Mühlen. "Attaching and effacing pathogens: the effector ABC of immune subversion." Future Microbiology 15, no. 10 (July 2020): 945–58. http://dx.doi.org/10.2217/fmb-2019-0274.

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The innate immune response resembles an essential barrier to bacterial infection. Many bacterial pathogens have, therefore, evolved mechanisms to evade from or subvert the host immune response in order to colonize, survive and multiply. The attaching and effacing pathogens enteropathogenic Escherichia coli, enterohaemorrhagic E. coli, Escherichia albertii and Citrobacter rodentium are Gram-negative extracellular gastrointestinal pathogens. They use a type III secretion system to inject effector proteins into the host cell to manipulate a variety of cellular processes. Over the last decade, considerable progress was made in identifying and characterizing the effector proteins of attaching and effacing pathogens that are involved in the inhibition of innate immune signaling pathways, in determining their host cell targets and elucidating the mechanisms they employ. Their functions will be reviewed here.

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25

Kroemer, Guido, and Laurence Zitvogel. "Subversion of calreticulin exposure as a strategy of immune escape." Cancer Cell 39, no. 4 (April 2021): 449–51. http://dx.doi.org/10.1016/j.ccell.2021.01.014.

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26

Wodarz, Dominik, and Martin A. Nowak. "Evolutionary dynamics of HIV-induced subversion of the immune response." Immunological Reviews 168, no. 1 (April 1999): 75–98. http://dx.doi.org/10.1111/j.1600-065x.1999.tb01284.x.

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27

CARRERO, J., and E. UNANUE. "Lymphocyte apoptosis as an immune subversion strategy of microbial pathogens." Trends in Immunology 27, no. 11 (November 2006): 497–503. http://dx.doi.org/10.1016/j.it.2006.09.005.

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28

Du, Gangjun, Yinghui Liu, Jiahuan Li, Weijie Liu, Yingying Wang, and Hong Li. "Hypothermic microenvironment plays a key role in tumor immune subversion." International Immunopharmacology 17, no. 2 (October 2013): 245–53. http://dx.doi.org/10.1016/j.intimp.2013.06.018.

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29

Hajishengallis, George, and Patricia I. Diaz. "Porphyromonas gingivalis: Immune Subversion Activities and Role in Periodontal Dysbiosis." Current Oral Health Reports 7, no. 1 (January 10, 2020): 12–21. http://dx.doi.org/10.1007/s40496-020-00249-3.

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30

Lang, Christine, Uwe Groß, and Carsten G. K. Lüder. "Subversion of innate and adaptive immune responses by Toxoplasma Gondii." Parasitology Research 100, no. 2 (October 6, 2006): 191–203. http://dx.doi.org/10.1007/s00436-006-0306-9.

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31

Parrish, James M., Manasi Soni, and Rahul Mittal. "Subversion of host immune responses by otopathogens during otitis media." Journal of Leukocyte Biology 106, no. 4 (May 10, 2019): 943–56. http://dx.doi.org/10.1002/jlb.4ru0119-003r.

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32

Kondoh, Nobuo, Masako Mizuno-Kamiya, Eiji Takayama, Harumi Kawati, Naoki Umemura, Yutaka Yamazaki, Kenji Mitsudo, and Iwai Tohnai. "Perspectives of Immune Suppression in the Tumor Microenvironment Promoting Oral Malignancy." Open Dentistry Journal 12, no. 1 (June 20, 2018): 455–65. http://dx.doi.org/10.2174/1874210601812010455.

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Introduction:In order to survive, cancers control immune systems and evade immune detection using mediators consisting of immune checkpoint molecules and cellular systems associated with immune suppression.Methodology:During the development of cancer and chronic infections, the immune checkpoints and cellular components including regulatory T cells, myeloid derived suppressor cells and cancer associated fibroblasts are often enhanced as a mechanism of immune subversion and have therefore become very important therapeutic targets.Conclusion:In this review, we will discuss the complexity of immune-suppressive mechanisms in the tumor milieu of cancers, including oral malignancy.

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33

Chu, Timothy H., Camille Khairallah, Jason Shieh, Rhea Cho, Zhijuan Qiu, Yue Zhang, Onur Eskiocak, et al. "γδ T cell IFNγ production is directly subverted by Yersinia pseudotuberculosis outer protein YopJ in mice and humans." PLOS Pathogens 17, no. 12 (December 6, 2021): e1010103. http://dx.doi.org/10.1371/journal.ppat.1010103.

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Yersinia pseudotuberculosis is a foodborne pathogen that subverts immune function by translocation of Yersinia outer protein (Yop) effectors into host cells. As adaptive γδ T cells protect the intestinal mucosa from pathogen invasion, we assessed whether Y. pseudotuberculosis subverts these cells in mice and humans. Tracking Yop translocation revealed that the preferential delivery of Yop effectors directly into murine Vγ4 and human Vδ2+ T cells inhibited anti-microbial IFNγ production. Subversion was mediated by the adhesin YadA, injectisome component YopB, and translocated YopJ effector. A broad anti-pathogen gene signature and STAT4 phosphorylation levels were inhibited by translocated YopJ. Thus, Y. pseudotuberculosis attachment and translocation of YopJ directly into adaptive γδ T cells is a major mechanism of immune subversion in mice and humans. This study uncovered a conserved Y. pseudotuberculosis pathway that subverts adaptive γδ T cell function to promote pathogenicity.

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34

Rothschild, Ethan, and Debabrata Banerjee. "Subverting Subversion: A Review on the Breast Cancer Microenvironment and Therapeutic Opportunities." Breast Cancer: Basic and Clinical Research 9s2 (January 2015): BCBCR.S29423. http://dx.doi.org/10.4137/bcbcr.s29423.

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This review combines the recent research on the subject of tumor immunology and methods of correcting the immune system's reaction to the tumor microenvironment while impeding the survival and growth of tumor cells, with a focus on breast cancer. Induction of hypoxia-inducible genes in the microenvironment leads to lowering of its pH. This impedes the adaptive immune response and acts to recruit cells of the immune system, which suppress the immune response. Regulatory T-cells (Tregs), myeloid-derived suppressor cells (MDSCs), and their derivatives coordinate an anti-autoimmunity response and a healing response in concert with tumor-secreted cytokines, enzymes, and antigens. Together, they suppress a proper immune reaction to tumor cells and promote cellular reproduction ( Fig. 1 ). In addition, the hypoxia-inducible response and components of the tumor microenvironment such as cancer-associated fibroblasts (CAFs) also create an ideal environment for tumor growth and metastasis via neoangiogenesis and increased motility. Broad-spectrum chemotherapy drugs are problematic as breast cancer cells develop resistance through selective loss of a novel target and downregulation of apoptotic factors. A better understanding of the tumor microenvironment offers new therapeutic opportunities to rescue the immune response, inhibit cancer cell growth pathways, and subvert the tumor microenvironment with little toxicity and side effects.

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35

Zelazowska, Monika A., Kevin McBride, and Laurie T. Krug. "Dangerous Liaisons: Gammaherpesvirus Subversion of the Immunoglobulin Repertoire." Viruses 12, no. 8 (July 23, 2020): 788. http://dx.doi.org/10.3390/v12080788.

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A common biologic property of the gammaherpesviruses Epstein–Barr Virus and Kaposi sarcoma herpesvirus is their use of B lymphocytes as a reservoir of latency in healthy individuals that can undergo oncogenic transformation later in life. Gammaherpesviruses (GHVs) employ an impressive arsenal of proteins and non-coding RNAs to reprogram lymphocytes for proliferative expansion. Within lymphoid tissues, the germinal center (GC) reaction is a hub of B cell proliferation and death. The goal of a GC is to generate and then select for a pool of immunoglobulin (Ig) genes that will provide a protective humoral adaptive immune response. B cells infected with GHVs are detected in GCs and bear the hallmark signatures of the mutagenic processes of somatic hypermutation and isotype class switching of the Ig genes. However, data also supports extrafollicular B cells as a reservoir engaged by GHVs. Next-generation sequencing technologies provide unprecedented detail of the Ig sequence that informs the natural history of infection at the single cell level. Here, we review recent reports from human and murine GHV systems that identify striking differences in the immunoglobulin repertoire of infected B cells compared to their uninfected counterparts. Implications for virus biology, GHV-associated cancers, and host immune dysfunction will be discussed.

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36

Elliott, Jabari I., Xiaoli Wang, Sytse J. Piersma, Christopher A. Nelson, Wayne M. Yokoyama, and Daved H. Fremont. "Poxvirus subversion of B7-mediated T cell co-stimulation." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 126.18. http://dx.doi.org/10.4049/jimmunol.200.supp.126.18.

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Abstract Poxviruses encode a broad array of proteins that serve to undermine host immune defenses. Our group has been investigating a large sequence-diverse family of secreted poxvirus proteins that appear to share a conserved beta-sandwich fold, but differ in their binding specificities. Host proteins discovered to interact with this viral protein family include: chemokines, GM-CSF, IL-2, MHC class I, and GAGs. We have termed members of this superfamily; Poxvirus Immune Evasion (PIE) proteins, and there appears to be at least 20 distinct subfamilies. As it turns out, cowpox virus (CPXV BR) contains 10 PIE proteins, one of which is secreted from virally infected cells and specifically binds B7.1 (CD80) and B7.2 (CD86), two membrane proteins expressed on professional antigen presenting cells and activated T cells. We have termed this viral protein B7 Response Modifier (BRM) and demonstrated that it competes with the CD28 as well as CTLA4 receptors expressed on T-cells for binding to B7 proteins. However, at low concentration, BRM competes primarily with CD28 for binding to B7.2, consistent with the idea that cowpox uses BRM to undermine T cell activation but not checkpoint control. Quantitative interaction analysis reveals that BRM binds the ectodomain of B7 proteins with higher affinity than that reported for CD28 or CTLA-4. Functionally, BRM can potently disrupt T-cell proliferation and IL2 production co-stimulated by B7 proteins. Furthermore, supernatants of wild-type but not BRM deleted CPXV are capable of suppressing B7.2-mediated T-cell activation. In sum, our findings define a novel mechanism of viral immune evasion that highlights the role of CD28 co-stimulation in host defense of poxvirus infections.

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37

Murphy, Philip M. "Viral exploitation and subversion of the immune system through chemokine mimicry." Nature Immunology 2, no. 2 (February 2001): 116–22. http://dx.doi.org/10.1038/84214.

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38

Lambert, Henrik, and Antonio Barragan. "Modelling parasite dissemination: host cell subversion and immune evasion byToxoplasma gondii." Cellular Microbiology 12, no. 3 (March 2010): 292–300. http://dx.doi.org/10.1111/j.1462-5822.2009.01417.x.

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39

Kottke, Tim, Laura Evgin, Kevin G. Shim, Diana Rommelfanger, Nicolas Boisgerault, Shane Zaidi, Rosa Maria Diaz, et al. "Subversion of NK-cell and TNFα Immune Surveillance Drives Tumor Recurrence." Cancer Immunology Research 5, no. 11 (October 15, 2017): 1029–45. http://dx.doi.org/10.1158/2326-6066.cir-17-0175.

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40

Foureau, David, Qing Zhang, Lawrence J. Druhan, Nury M. Steuerwald, Fei Guo, Elizabeth Jandrisevits, Belinda R. Avalos, Danyu Sun, Ryan Jacobs, and Nilanjan Ghosh. "NF-κb / STAT3 Signaling Pathway Collaboration in Diffuse Large B-Cell Lymphoma (DLBCL) Cell-of-Origin (COO) Subtypes: Resolution of Myeloid Subversion By Standard Induction Chemotherapy." Blood 128, no. 22 (December 2, 2016): 4133. http://dx.doi.org/10.1182/blood.v128.22.4133.4133.

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Abstract Background. Germinal center B-cell (GCB) and activated B-cell (ABC) are two main cell-of-origin (COO) subtypes of diffuse large B-cell lymphomas(DLBCL). Patients presenting with the ABC-DLBCL subtype have inferior outcomes following standard rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone (R-CHOP) therapy. Since ABC-DLBCL phenotype is characterized by marked activation of nuclear factor kappa B (NF-κB) signaling pathway, we hypothesized that inferior outcomes of patients with this COO subgroup treated with standard therapy were due to unresolved innate immune bias or myeloid subversion. Methods. Immunological profiles were established for 23 newly diagnosed DLBCL patients (n=13 ABC, n=10 GCB) prior to induction therapy (R-CHOP or R-EPOCH). Serum concentrations of 25 cytokines, chemokines and growth factors, were quantified by a multiplex protein assay. Peripheral distribution of myeloid cells (CD11b+ CD33+), myeloid maturation (HLA-DR+/-IL-4R+/-) and myeloid subversion [monocytic (m) and granulocytic (g) myeloid-derived suppressor cells (MDSCs)] were established by flow cytometry. These 31 immune variables were reassessed after completion of induction therapy for 16 DLBCL patients (n=10 ABC, n=6 GCB). Linear regression was used to determine the association between each tested variable and COO or modified international prognosis index (R-IPI). Unsupervised hierarchical cluster analysis was then applied to diagnosis samples with the selected variables that were differentially expressed between ABC- and GCB-DLBCL subtypes (p<0.1) using complete linkage and Euclidean distances. Paired t-test was used to compare each immune variable before and after chemotherapy. Results. At diagnosis, 14 of 25 immune analytes transcriptionally regulated by NF-κB were equally expressed between the two COO subgroups. ABC-DLBCL has lower PDGF-bb serum concentrations (p=.008). Two immune analytes regulated by the STAT3 signaling pathway, INFg-induced protein 10 (IP10) and IL-9 are differentially expressed among the two COO. While STAT3 positively regulates IP10, leading to elevated IP10 serum concentrations in ABC-DLBCL patients (p=0.003), it negatively regulates IL-9 leading to reduced IL-9 serum concentrations in this COO-subtype (p=0.05). Hierarchical clustering analysis of DLBCL patients at diagnosis shows that 9/13 ABC-DLBCL patients exhibit this STAT3 signature. STAT3 signaling pathway activation is also associated with myeloid immune subversion promoting gMDSC expansion in the ABC-DLBCL subtype (p=0.05). No correlations could be established between immunological bias at diagnosis in the 2 COO subtypes and R-IPI. Among the 16 patients who have completed chemotherapy (n=12 R-CHOP & n=4 R-EPOCH), none were refractory to induction therapy. ABC-DLBCL subtypes displayed the most profound immunological alterations compared with GCB-DLBCL, with decrease in serum concentrations of 7 immune analytes regulated by NF-κB (IL-6, IL-8, MIP1a, MIP1b, IL-1ra, GM-CSF and PDGF-bb). Standard chemotherapy leads to resolution of myeloid subversion and STAT3 bias as exemplified by normalization of the distribution of gMDSCs and IP10 and IL-9 serum concentrations between the two COO subgroups. Conclusion. Immune profiling of newly diagnosed DLBCL patients identified distinct biological signatures associated with COO subtypes. Highly enriched NF-κB signaling activation in ABC-DLBCL patients was associated with a STAT3-driven cytokine signature (NF-κB/STAT3 collaboration) and myeloid subversion. Standard induction chemotherapy normalized immunological bias across COO DLBCL subgroups. Longer follow up with clinical correlations are in progress to determine the significance of myeloid subversion and the NF-kB/STAT3 signature at diagnosis in DLBCL. Disclosures Avalos: Seattle Genetics: Membership on an entity's Board of Directors or advisory committees. Jacobs:Magellan Health: Consultancy; Pharmacyclics: Consultancy, Speakers Bureau. Ghosh:Bristol Myers Squibb: Consultancy, Honoraria, Research Funding; Gilead: Honoraria, Speakers Bureau; Janssen: Consultancy, Honoraria, Research Funding, Speakers Bureau; SGN: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding; AbbVie: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Speakers Bureau; Pharmacyclics LLC, an AbbVie Company: Consultancy, Honoraria, Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Celgene: Consultancy, Honoraria, Research Funding, Speakers Bureau; Genentech: Research Funding; TG Therapeutics: Research Funding.

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41

Bouvier, Marlene, Lenong Li, and Hui Deng. "Subversion of antigen presentation by Adenoviruses." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 99.26. http://dx.doi.org/10.4049/jimmunol.200.supp.99.26.

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Abstract The cell-surface presentation of viral antigens by MHC class I molecules to CD8+ T-cells is critical for eliminating virus-infected cells. In turn, viruses have evolved numerous strategies to interfere with the generation and presentation of class I antigens. Human adenoviruses (Ads) comprise more than 70 different types classified into seven species (A to G); Ad infections cause diseases of the respiratory track (species B, C, and E), eyes (species D), and gastrointestinal track (species F). Ads encode the E3-19K protein that targets MHC class I molecules for retention in the endoplasmic reticulum of infected cells, thereby suppressing cell-surface presentation of Ad-derived antigens. In recent years, we determined the x-ray structures of Ad2 (species C) and Ad4 (species E) E3-19K bound to HLA-A2, which together with biochemical and functional data allowed to explain the mechanism of immunomodulation. Interestingly, in comparison to other Ads, species F Ads lack a gene for the common E3-19K protein and instead have two unique and uncharacterized genes, E3-19.4K and -31.6K. We are using a biochemical and functional approach to investigate how species F Ads modulate various cell surface immune proteins, including MHC I molecules, and what role of E3-19.4K and -31.6K proteins play in these effects.

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Aquino, Rafael S., Yvonne Hui-Fang Teng, and Pyong Woo Park. "Glycobiology of syndecan-1 in bacterial infections." Biochemical Society Transactions 46, no. 2 (March 9, 2018): 371–77. http://dx.doi.org/10.1042/bst20170395.

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Syndecan-1 (Sdc1) is a major cell surface heparan sulfate (HS) proteoglycan of epithelial cells, a cell type targeted by many bacterial pathogens early in their pathogenesis. Loss of Sdc1 in mice is a gain-of-function mutation that significantly decreases the susceptibility to several bacterial infections, suggesting that subversion of Sdc1 is an important virulence strategy. HS glycosaminoglycan (GAG) chains of cell surface Sdc1 promote bacterial pathogenesis by facilitating the attachment of bacteria to host cells. Engagement of cell surface Sdc1 HS chains by bacterial adhesins transmits signal through the highly conserved Sdc1 cytoplasmic domain, which can lead to uptake of intracellular bacterial pathogens. On the other hand, several bacteria that do not require Sdc1 for their attachment and invasion stimulate Sdc1 shedding and exploit the capacity of Sdc1 ectodomain HS GAGs to disarm innate defense mechanisms to evade immune clearance. Recent data suggest that select HS sulfate motifs, and not the overall charge of HS, are important in the inhibition of innate immune mechanisms. Here, we discuss several examples of Sdc1 subversion in bacterial infections.

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Chu, Timothy H., Camille Khairallah, Jason Shieh, Rhea Cho, Zhijuan Qiu, Yue Zhang, Indralatha Jayatilaka, et al. "Adaptive γδ T cell function is directly subverted by the Yersinia pseudotuberculosis outer protein YopJ." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 99.04. http://dx.doi.org/10.4049/jimmunol.206.supp.99.04.

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Abstract Vγ4 T cells are an unconventional subset of T cells that protect the intestinal mucosa from pathogen invasion and capable of anamnestic responses. Yersinia pseudotuberculosis (Yptb) is a foodborne pathogen that invades through the intestinal mucosa and subverts immune function by translocation of Yersiniaouter protein (Yop) effectors into target cells. In this study, we evaluated the response of adaptive Vγ4 T cells to Yptb to determine if adaptive γδ T cells are a target of immune subversion. Tracking Yptb translocation of Yop effectors through a FRET-based reporter assay revealed targeted and preferential delivery of Yop effectors directly into adaptive γδ T cells inhibited anti-microbial IFNγ production. Using a series of recombinant Yptb deficient or defective in numerous pathogenicity genes revealed that direct subversion of the adaptive γδ T cell IFNγ response was mediated by the adhesion molecule YadA, the injectosome component YopB, and the YopJ effector. Thus, Yptb attachment and translocation of YopJ directly into adaptive γδ T cells is a major mechanism of γδ T cell subversion. RNA-Seq of adaptive γδ T cells revealed that a broad anti-pathogen gene signature was inhibited by translocation of YopJ and suggested a role of the STAT4 pathway in this process. Indeed, IL-12p40 promoted the adaptive γδ T cell IFNγ response and YopJ limited STAT4 phosphorylation levels. Importantly, circulating human Vδ2+T cells were similarly targeted and inhibited by the YopJ effector, highlighting a novel and conserved Yptb pathway that subverts adaptive γδ T cell function.

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van den Elsen, Jean, Abhishek Upadhyay, Julia Burman, Elisa Leung, Elisabeth Clark, David Isenman, and Stefan Bagby. "Structure–function analysis of the novel Staphylococcus aureus immune subversion protein Sbi." Molecular Immunology 45, no. 16 (October 2008): 4119. http://dx.doi.org/10.1016/j.molimm.2008.08.071.

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Hahn, Young S. "Subversion of immune responses by hepatitis C virus: immunomodulatory strategies beyond evasion?" Current Opinion in Immunology 15, no. 4 (August 2003): 443–49. http://dx.doi.org/10.1016/s0952-7915(03)00076-1.

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Tazzyman, Simon, Hanan Niaz, and Craig Murdoch. "Neutrophil-mediated tumour angiogenesis: Subversion of immune responses to promote tumour growth." Seminars in Cancer Biology 23, no. 3 (June 2013): 149–58. http://dx.doi.org/10.1016/j.semcancer.2013.02.003.

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Arbibe, Laurence. "Immune subversion by chromatin manipulation: a new face of hostbacterial pathogen interaction." Cellular Microbiology 10, no. 8 (August 2008): 1582–90. http://dx.doi.org/10.1111/j.1462-5822.2008.01170.x.

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Le Negrate, Gaëlle. "Subversion of innate immune responses by bacterial hindrance of NF-κB pathway." Cellular Microbiology 14, no. 2 (November 23, 2011): 155–67. http://dx.doi.org/10.1111/j.1462-5822.2011.01719.x.

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Mohan, Gopi S., Wenfang Li, Ling Ye, Richard W. Compans, and Chinglai Yang. "Antigenic Subversion: A Novel Mechanism of Host Immune Evasion by Ebola Virus." PLoS Pathogens 8, no. 12 (December 13, 2012): e1003065. http://dx.doi.org/10.1371/journal.ppat.1003065.

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Snyder, Greg. "G-108 Subversion of innate immune responses by microbial TIR interacting proteins." JAIDS Journal of Acquired Immune Deficiency Syndromes 67 (November 2014): 71. http://dx.doi.org/10.1097/01.qai.0000456171.89019.3d.

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