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https://www.readbyqxmd.com/read/27909702/complement-inhibition-enables-tumor-delivery-of-lcmv-glycoprotein-pseudotyped-viruses-in-the-presence-of-antiviral-antibodies
#1
Laura Evgin, Carolina S Ilkow, Marie-Claude Bourgeois-Daigneault, Christiano Tanese de Souza, Lawton Stubbert, Michael S Huh, Victoria A Jennings, Monique Marguerie, Sergio A Acuna, Brian A Keller, Charles Lefebvre, Theresa Falls, Fabrice Le Boeuf, Rebecca A Auer, John D Lambris, J Andrea McCart, David F Stojdl, John C Bell
The systemic delivery of therapeutic viruses, such as oncolytic viruses or vaccines, is limited by the generation of neutralizing antibodies. While pseudotyping of rhabdoviruses with the lymphocytic choriomeningitis virus glycoprotein has previously allowed for multiple rounds of delivery in mice, this strategy has not translated to other animal models. For the first time, we provide experimental evidence that antibodies generated against the lymphocytic choriomeningitis virus glycoprotein mediate robust complement-dependent viral neutralization via activation of the classical pathway...
2016: Molecular Therapy Oncolytics
https://www.readbyqxmd.com/read/27782328/more-than-complementing-tolls-complement-toll-like-receptor-synergy-and-crosstalk-in-innate-immunity-and-inflammation
#2
REVIEW
George Hajishengallis, John D Lambris
Complement and Toll-like receptors (TLRs) play key roles in the host immune response and are swiftly activated by infection or other types of immunological stress. This review focuses on the capacity of complement and TLRs to engage in signaling crosstalk, ostensibly to coordinate immune and inflammatory responses through synergistic or antagonistic (regulatory) interactions. However, overactivation or dysregulation of either system may lead-often synergistically-to exaggerated inflammation and host tissue injury...
November 2016: Immunological Reviews
https://www.readbyqxmd.com/read/27782325/complement-component-c3-the-swiss-army-knife-of-innate-immunity-and-host-defense
#3
REVIEW
Daniel Ricklin, Edimara S Reis, Dimitrios C Mastellos, Piet Gros, John D Lambris
As a preformed defense system, complement faces a delicate challenge in providing an immediate, forceful response to pathogens even at first encounter, while sparing host cells in the process. For this purpose, it engages a tightly regulated network of plasma proteins, cell surface receptors, and regulators. Complement component C3 plays a particularly versatile role in this process by keeping the cascade alert, acting as a point of convergence of activation pathways, fueling the amplification of the complement response, exerting direct effector functions, and helping to coordinate downstream immune responses...
November 2016: Immunological Reviews
https://www.readbyqxmd.com/read/27782322/preformed-mediators-of-defense-gatekeepers-enter-the-spotlight
#4
Daniel Ricklin, John D Lambris
No abstract text is available yet for this article.
November 2016: Immunological Reviews
https://www.readbyqxmd.com/read/27782321/protection-of-host-cells-by-complement-regulators
#5
REVIEW
Christoph Q Schmidt, John D Lambris, Daniel Ricklin
The complement cascade is an ancient immune-surveillance system that not only provides protection from pathogen invasion but has also evolved to participate in physiological processes to maintain tissue homeostasis. The alternative pathway (AP) of complement activation is the evolutionarily oldest part of this innate immune cascade. It is unique in that it is continuously activated at a low level and arbitrarily probes foreign, modified-self, and also unaltered self-structures. This indiscriminate activation necessitates the presence of preformed regulators on autologous surfaces to spare self-cells from the undirected nature of AP activation...
November 2016: Immunological Reviews
https://www.readbyqxmd.com/read/27709886/the-dynamics-behind-the-affinity-controling-heme-gas-affinity-via-geminate-recombination-and-heme-propionate-conformation-in-the-no-carrier-cytochrome-c
#6
Colin R Andrew, Olga N Petrova, Isabelle Lamarre, Jean-Christophe Lambry, Fabrice Rappaport, Michel Negrerie
Nitric oxide (NO) sensors are heme proteins which may also bind CO and O2. Control of heme-gas affinity and their discrimination are achieved by the structural properties and reactivity of the heme and its distal and proximal environments, leading to several energy barriers. In the bacterial NO-sensor cytochrome c' from Alcaligenes xylosoxidans (AXCP), the single Leu16Ala distal mutation boosts the affinity for gas ligands by a remarkable 106-108-fold, transforming AXCP from one of the lowest affinity gas binding proteins to one of the highest...
October 6, 2016: ACS Chemical Biology
https://www.readbyqxmd.com/read/27677785/complement-c3-inhibitor-cp40-attenuates-xenoreactions-in-pig%C3%A2-hearts-perfused-with-human-blood
#7
Jan-Michael Abicht, Ioannis Kourtzelis, Bruno Reichart, Sophia Koutsogiannaki, Alexandra Primikyri, John D Lambris, Triantafyllos Chavakis, Lesca Holdt, Alexander Kind, Sonja Guethoff, Tanja Mayr
BACKGROUND: The complement system plays a crucial role in acute xenogeneic reactions after cardiac transplantation. We used an ex vivo perfusion model to investigate the effect of Cp40, a compstatin analog and potent inhibitor of complement at the level of C3. METHODS: Fifteen wild-type pig hearts were explanted, cardiopleged, and reperfused ex vivo after 150 minutes of cold ischemia. Hearts were challenged in a biventricular working heart mode to evaluate cardiac perfusion and function...
September 27, 2016: Xenotransplantation
https://www.readbyqxmd.com/read/27546448/compstatin-cp40-blocks-hematin-mediated-deposition-of-c3b-fragments-on-erythrocytes-implications-for-treatment-of-malarial-anemia
#8
Margaret A Lindorfer, Erika M Cook, Edimara S Reis, Daniel Ricklin, Antonio M Risitano, John D Lambris, Ronald P Taylor
During malarial anemia, 20 uninfected red blood cells (RBCs) are destroyed for every RBC infected by Plasmodium falciparum (Pf). Increasing evidence indicates an important role for complement in destruction of uninfected RBCs. Products of RBC lysis induced by Pf, including the digestive vacuole and hematin, activate complement and promote C3 fragment deposition on uninfected RBCs. C3-opsonized cells are then subject to extravascular destruction mediated by fixed tissue macrophages which express receptors for C3 fragments...
October 2016: Clinical Immunology: the Official Journal of the Clinical Immunology Society
https://www.readbyqxmd.com/read/27535705/high-fat-diet-induced-complement-activation-mediates-intestinal-inflammation-and-neoplasia-independent-of-obesity
#9
Stephanie K Doerner, Edimara S Reis, Elaine S Leung, Justine S Ko, Jason D Heaney, Nathan A Berger, John D Lambris, Joseph H Nadeau
: Obesity and related metabolic disturbances are closely associated with pathologies that represent a significant burden to global health. Epidemiological and molecular evidence links obesity and metabolic status with inflammation and increased risk of cancer. Here, using a mouse model of intestinal neoplasia and strains that are susceptible or resistant to diet-induced obesity, it is demonstrated that high-fat diet-induced inflammation, rather than obesity or metabolic status, is associated with increased intestinal neoplasia...
October 2016: Molecular Cancer Research: MCR
https://www.readbyqxmd.com/read/27522923/complement-therapeutics
#10
EDITORIAL
Daniel Ricklin, John D Lambris
No abstract text is available yet for this article.
June 2016: Seminars in Immunology
https://www.readbyqxmd.com/read/27511733/systems-analysis-of-the-complement-induced-priming-phase-of-liver-regeneration
#11
Jun S Min, Robert A DeAngelis, Edimara S Reis, Shakti Gupta, Mano R Maurya, Charles Evans, Arun Das, Charles Burant, John D Lambris, Shankar Subramaniam
Liver regeneration is a well-orchestrated process in the liver that allows mature hepatocytes to reenter the cell cycle to proliferate and replace lost or damaged cells. This process is often impaired in fatty or diseased livers, leading to cirrhosis and other deleterious phenotypes. Prior research has established the role of the complement system and its effector proteins in the progression of liver regeneration; however, a detailed mechanistic understanding of the involvement of complement in regeneration is yet to be established...
September 15, 2016: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/27353192/from-orphan-drugs-to-adopted-therapies-advancing-c3-targeted-intervention-to-the-clinical-stage
#12
REVIEW
Dimitrios C Mastellos, Edimara S Reis, Despina Yancopoulou, George Hajishengallis, Daniel Ricklin, John D Lambris
Complement dysregulation is increasingly recognized as an important pathogenic driver in a number of clinical disorders. Complement-triggered pathways intertwine with key inflammatory and tissue destructive processes that can either increase the risk of disease or exacerbate pathology in acute or chronic conditions. The launch of the first complement-targeted drugs in the clinic has undeniably stirred the field of complement therapeutic design, providing new insights into complement's contribution to disease pathogenesis and also helping to leverage a more personalized, comprehensive approach to patient management...
October 2016: Immunobiology
https://www.readbyqxmd.com/read/27321574/new-milestones-ahead-in-complement-targeted-therapy
#13
REVIEW
Daniel Ricklin, John D Lambris
The complement system is a powerful effector arm of innate immunity that typically confers protection from microbial intruders and accumulating debris. In many clinical situations, however, the defensive functions of complement can turn against host cells and induce or exacerbate immune, inflammatory, and degenerative conditions. Although the value of inhibiting complement in a therapeutic context has long been recognized, bringing complement-targeted drugs into clinical use has proved challenging. This important milestone was finally reached a decade ago, yet the clinical availability of complement inhibitors has remained limited...
June 2016: Seminars in Immunology
https://www.readbyqxmd.com/read/27211870/complement-in-disease-a-defence-system-turning-offensive
#14
REVIEW
Daniel Ricklin, Edimara S Reis, John D Lambris
Although the complement system is primarily perceived as a host defence system, a more versatile, yet potentially more harmful side of this innate immune pathway as an inflammatory mediator also exists. The activities that define the ability of the complement system to control microbial threats and eliminate cellular debris - such as sensing molecular danger patterns, generating immediate effectors, and extensively coordinating with other defence pathways - can quickly turn complement from a defence system to an aggressor that drives immune and inflammatory diseases...
July 2016: Nature Reviews. Nephrology
https://www.readbyqxmd.com/read/27183616/properdin-mediated-c5a-production-enhances-stable-binding-of-platelets-to-granulocytes-in-human-whole-blood
#15
Adam Z Blatt, Gurpanna Saggu, Koustubh V Kulkarni, Claudio Cortes, Joshua M Thurman, Daniel Ricklin, John D Lambris, Jesus G Valenzuela, Viviana P Ferreira
Enhanced levels of platelet/granulocyte aggregates (PGAs) are found in patients suffering from many different inflammatory vascular diseases, and their formation in animal models of vascular disease is associated with increased thromboinflammation and worsened outcomes. The complement system, a part of the innate immune system, influences PGA formation, but the mechanisms for its effects are unknown. In this study, we have defined complement-mediated mechanisms that enhance PGA formation in human whole blood stimulated with thrombin receptor-activating peptide (TRAP) using ex vivo flow cytometry assays...
June 1, 2016: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/27081768/differential-capacity-for-complement-receptor-mediated-immune-evasion-by-porphyromonas-gingivalis-depending-on-the-type-of-innate-leukocyte
#16
George Hajishengallis, Jennifer L Krauss, Ravi Jotwani, John D Lambris
The complement system plays a central role in immunity and inflammation, although certain pathogens can exploit complement to undermine protective immunity. In this context, the periodontal keystone pathogen Porphyromonas gingivalis (Pg) was previously shown by our group to evade killing by neutrophils or macrophages through exploitation of complement C5a receptor 1 (C5aR1) and complement receptor-3 (CR3). Here, we examined whether Pg uses complement receptors to also subvert killing by dendritic cells. In line with earlier independent studies, intracellular viable Pg bacteria could be recovered from mouse bone marrow-derived dendritic cells (BMDC) or human monocyte-derived dendritic cells (MDDC) exposed to the pathogen...
April 15, 2016: Molecular Oral Microbiology
https://www.readbyqxmd.com/read/27041467/control-of-the-collective-migration-of-enteric-neural-crest-cells-by-the-complement-anaphylatoxin-c3a-and-n-cadherin
#17
Florence Broders-Bondon, Perrine Paul-Gilloteaux, Elodie Gazquez, Julie Heysch, Matthieu Piel, Roberto Mayor, John D Lambris, Sylvie Dufour
We analyzed the cellular and molecular mechanisms governing the adhesive and migratory behavior of enteric neural crest cells (ENCCs) during their collective migration within the developing mouse gut. We aimed to decipher the role of the complement anaphylatoxin C3a during this process, because this well-known immune system attractant has been implicated in cephalic NCC co-attraction, a process controlling directional migration. We used the conditional Ht-PA-cre transgenic mouse model allowing a specific ablation of the N-cadherin gene and the expression of a fluorescent reporter in migratory ENCCs without affecting the central nervous system...
June 1, 2016: Developmental Biology
https://www.readbyqxmd.com/read/27021500/complement-inhibition-in-pre-clinical-models-of-periodontitis-and-prospects-for-clinical-application
#18
REVIEW
George Hajishengallis, Evlambia Hajishengallis, Tetsuhiro Kajikawa, Baomei Wang, Despina Yancopoulou, Daniel Ricklin, John D Lambris
Periodontitis is a dysbiotic inflammatory disease leading to the destruction of the tooth-supporting tissues. Current therapies are not always effective and this prevalent oral disease continues to be a significant health and economic burden. Early clinical studies have associated periodontitis with elevated complement activity. Consistently, subsequent genetic and pharmacological studies in rodents have implicated the central complement component C3 and downstream signaling pathways in periodontal host-microbe interactions that promote dysbiosis and inflammatory bone loss...
June 2016: Seminars in Immunology
https://www.readbyqxmd.com/read/27013439/regulators-of-complement-activity-mediate-inhibitory-mechanisms-through-a-common-c3b-binding-mode
#19
Federico Forneris, Jin Wu, Xiaoguang Xue, Daniel Ricklin, Zhuoer Lin, Georgia Sfyroera, Apostolia Tzekou, Elena Volokhina, Joke Cm Granneman, Richard Hauhart, Paula Bertram, M Kathryn Liszewski, John P Atkinson, John D Lambris, Piet Gros
Regulators of complement activation (RCA) inhibit complement-induced immune responses on healthy host tissues. We present crystal structures of human RCA (MCP, DAF, and CR1) and a smallpox virus homolog (SPICE) bound to complement component C3b. Our structural data reveal that up to four consecutive homologous CCP domains (i-iv), responsible for inhibition, bind in the same orientation and extended arrangement at a shared binding platform on C3b. Large sequence variations in CCP domains explain the diverse C3b-binding patterns, with limited or no contribution of some individual domains, while all regulators show extensive contacts with C3b for the domains at the third site...
May 17, 2016: EMBO Journal
https://www.readbyqxmd.com/read/26977050/combined-inhibition-of-complement-and-cd14-attenuates-bacteria-induced-inflammation-in-human-whole-blood-more-efficiently-than-antagonizing-the-toll-like-receptor-4-md2-complex
#20
Alice Gustavsen, Stig Nymo, Anne Landsem, Dorte Christiansen, Liv Ryan, Harald Husebye, Corinna Lau, Søren E Pischke, John D Lambris, Terje Espevik, Tom E Mollnes
BACKGROUND: Single inhibition of the Toll-like receptor 4 (TLR4)-MD2 complex failed in treatment of sepsis. CD14 is a coreceptor for several TLRs, including TLR4 and TLR2. The aim of this study was to investigate the effect of single TLR4-MD2 inhibition by using eritoran, compared with the effect of CD14 inhibition alone and combined with the C3 complement inhibitor compstatin (Cp40), on the bacteria-induced inflammatory response in human whole blood. METHODS: Cytokines were measured by multiplex technology, and leukocyte activation markers CD11b and CD35 were measured by flow cytometry...
July 1, 2016: Journal of Infectious Diseases
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