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      1. Author :
        Ziegler, Annett; Soldner, Claudia; Lienenklaus, Stefan; Spanier, Julia; Trittel, Stephanie; Riese, Peggy; Kramps, Thomas; Weiss, Siegfried; Heidenreich, Regina; Jasny, Edith; Guzmán, Carlos A.; Kallen, Karl-Josef; Fotin-Mleczek, Mariola; Kalinke, Ulrich
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        The Journal of Immunology
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS; IVIS BLI in vivo
      12. Abstract :
        Among innovative adjuvants conferring a Th1-shift, RNAdjuvant is a promising candidate. This adjuvant consists of a 547-nt uncapped noncoding ssRNA containing polyU repeats that is stabilized by a cationic carrier peptide. Whereas vaccination of mice with an influenza subunit vaccine induced moderate virus-specific IgG1, vaccination together with RNAdjuvant significantly enhanced this IgG1 and additionally promoted the formation of IgG2b/c, which is indicative of Th1 responses. Furthermore, such sera neutralized influenza virus, whereas this effect was not detected upon vaccination with the subunit vaccine alone. Similarly, upon vaccination with virus-like particles displaying vesicular stomatitis virus G protein, RNAdjuvant promoted the formation of virus-specific IgG2b/c and enhanced neutralizing IgG responses to an extent that mice were protected against lethal virus infection. RNAdjuvant induced dendritic cells to upregulate activation markers and produce IFN-I. Although these effects were strictly TLR7 dependent, RNAdjuvant-mediated augmentation of vaccine responses needed concurrent TLR and RIG-I–like helicase signaling. This was indicated by the absence of the adjuvant effect in vaccinated MyD88−/−Cardif−/− mice, which are devoid of TLR (with the exception of TLR3) and RIG-I–like helicase signaling, whereas in vaccinated MyD88−/− mice the adjuvant effect was reduced. Notably, i.m. RNAdjuvant injection induced local IFN-I responses and did not induce systemic effects, implying good tolerability and a favorable safety profile for RNAdjuvant.%U http://www.jimmunol.org/content/jimmunol/early/2017/01/11/jimmunol.1601129.full.pdf
      13. URL :
        http://www.jimmunol.org/content/198/4/1595
      14. Call Number :
        PKI @ catherine.lautenschlager @ 13194
      15. Serial :
        13538
      1. Author :
        Zilio, Serena; Vella, Jennifer L.; De la Fuente, Adriana C.; Daftarian, Pirouz M.; Weed, Donald T.; Kaifer, Angel; Marigo, Ilaria; Leone, Kevin; Bronte, Vincenzo; Serafini, Paolo
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        The Journal of Immunology
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS; IVIS FLI in vivo
      12. Abstract :
        Myeloid cells play a key role in tumor progression and metastasis by providing nourishment and immune protection, as well as facilitating cancer invasion and seeding to distal sites. Although advances have been made in understanding the biology of these tumor-educated myeloid cells (TEMCs), their intrinsic plasticity challenges our further understanding of their biology. Indeed, in vitro experiments only mimic the in vivo setting, and current gene-knockout technologies do not allow the simultaneous, temporally controlled, and cell-specific silencing of multiple genes or pathways. In this article, we describe the 4PD nanoplatform, which allows the in vivo preferential transfection and in vivo tracking of TEMCs with the desired RNAs. This platform is based on the conjugation of CD124/IL-4Rα–targeting peptide with G5 PAMAM dendrimers as the loading surface and can convey therapeutic or experimental RNAs of interest. When injected i.v. in mice bearing CT26 colon carcinoma or B16 melanoma, the 4PD nanoparticles predominantly accumulate at the tumor site, transfecting intratumoral myeloid cells. The use of 4PD to deliver a combination of STAT3- and C/EBPβ-specific short hairpin RNA or miR-142-3p confirmed the importance of these genes and microRNAs in TEMC biology and indicates that silencing of both genes is necessary to increase the efficacy of immune interventions. Thus, the 4PD nanoparticle can rapidly and cost effectively modulate and assess the in vivo function of microRNAs and mRNAs in TEMCs.%U http://www.jimmunol.org/content/jimmunol/early/2017/04/07/jimmunol.1600833.full.pdf
      13. URL :
        http://www.jimmunol.org/content/198/10/4166
      14. Call Number :
        PKI @ catherine.lautenschlager @ 13657
      15. Serial :
        13536
      1. Author :
        Le Gars, Mathieu; Haustant, Michel; Klezovich-Bénard, Maria; Paget, Christophe; Trottein, François; Goossens, Pierre L.; Tournier, Jean-Nicolas
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2016
      5. Publication :
        The Journal of Immunology
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Ivis; Ivis Bli
      12. Abstract :
        Exogenous activation of invariant NKT (iNKT) cells by the superagonist α-galactosylceramide (α-GalCer) can protect against cancer, autoimmune diseases, and infections. In the current study, we investigated the effect of α-GalCer against Bacillus anthracis infection, the agent of anthrax. Using an experimental model of s.c. B. anthracis infection (an encapsulated nontoxigenic strain), we show that concomitant administration of α-GalCer delayed B. anthracis systemic dissemination and prolonged mouse survival. Depletion of subcapsular sinus CD169-positive macrophages by clodronate-containing liposome was associated with a lack of iNKT cell activation in the draining lymph nodes (dLNs) and prevented the protective effect of α-GalCer on bacterial dissemination out of the dLNs. Production of IFN-γ triggered chemokine (C-C motif) ligand 3 synthesis and recruitment of neutrophils in the dLNs, leading to the restraint of B. anthracis dissemination. Our data highlight a novel immunological pathway leading to the control of B. anthracis infection, a finding that might lead to improved therapeutics based on iNKT cells.
      13. URL :
        http://www.jimmunol.org/content/early/2016/09/07/jimmunol.1600830.abstract
      14. Call Number :
        PKI @ user @ 12338
      15. Serial :
        19760
      1. Author :
        Suzuki, Erika; Maverakis, Emanual; Sarin, Ritu; Bouchareychas, Laura; Kuchroo, Vijay K.; Nestle, Frank O.; Adamopoulos, Iannis E.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2016
      5. Publication :
        The Journal of Immunology
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Maestro
      12. Abstract :
        IL-17A has been strongly associated with epidermal hyperplasia in many cutaneous disorders. However, because IL-17A is mainly produced by αβ and γδT cells in response to IL-23, the role of T cells and IL-23 has overshadowed any IL-17A–independent actions. In this article, we report that IL-17A gene transfer induces epidermal hyperplasia in Il23r−/−Rag1−/−- and Tcrδ-deficient mice, which can be prevented by neutrophil depletion. Moreover, adoptive transfer of CD11b+Gr-1hi cells, after IL-17A gene transfer, was sufficient to phenocopy the disease. We further show that the IL-17A–induced pathology was prevented in transgenic mice with impaired neutrophil extracellular trap formation and/or neutrophils with conditional deletion of the master regulator of selective autophagy, Wdfy3. Our data demonstrate a novel T cell–independent mechanism that is associated with neutrophil extracellular trap formation and selective autophagy in IL-17A–mediated epidermal hyperplasia.%U http://www.jimmunol.org/content/jimmunol/early/2016/10/22/jimmunol.1600383.full.pdf
      13. URL :
        N/A
      14. Call Number :
        PKI @ catherine.lautenschlager @ 12575
      15. Serial :
        12912
      1. Author :
        Zhou, Qi; Uhlig, Katharina M.; Muth, Anke; Kimpel, Janine; Lévy, Camille; Münch, Robert C.; Seifried, Janna; Pfeiffer, Anett; Trkola, Alexandra; Coulibaly, Cheick; von Laer, Dorothee; Wels, Winfried S.; Hartwig, Udo F.; Verhoeyen, Els; Buchholz, Christian J.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2015
      5. Publication :
        The Journal of Immunology
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Ivis; Ivis Fli
      12. Abstract :
        Playing a central role in both innate and adaptive immunity, CD4+ T cells are a key target for genetic modifications in basic research and immunotherapy. In this article, we describe novel lentiviral vectors (CD4-LV) that have been rendered selective for human or simian CD4+ cells by surface engineering. When applied to PBMCs, CD4-LV transduced CD4+ but not CD4− cells. Notably, also unstimulated T cells were stably genetically modified. Upon systemic or intrasplenic administration into mice reconstituted with human PBMCs or hematopoietic stem cells, reporter gene expression was predominantly detected in lymphoid organs. Evaluation of GFP expression in organ-derived cells and blood by flow cytometry demonstrated exclusive gene transfer into CD4+ human lymphocytes. In bone marrow and spleen, memory T cells were preferentially hit. Toward therapeutic applications, we also show that CD4-LV can be used for HIV gene therapy, as well as for tumor therapy, by delivering chimeric Ag receptors. The potential for in vivo delivery of the FOXP3 gene was also demonstrated, making CD4-LV a powerful tool for inducible regulatory T cell generation. In summary, our work demonstrates the exclusive gene transfer into a T cell subset upon systemic vector administration opening an avenue toward novel strategies in immunotherapy.
      13. URL :
        http://www.jimmunol.org/content/early/2015/07/30/jimmunol.1500956.abstract
      14. Call Number :
        PKI @ user @ 9924
      15. Serial :
        20176
      1. Author :
        Terp, Mikkel G.; Olesen, Kristina A.; Arnspang, Eva C.; Lund, Rikke R.; Lagerholm, B. Christoffer; Ditzel, Henrik J.; Leth-Larsen, Rikke
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2013
      5. Publication :
        The Journal of Immunology
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS Imaging
      12. Abstract :
        Recent studies have shown that Abs that target the cell-surface enzyme CD73 (ecto-5′-nucleotidase) reduce growth of primary tumors and metastasis in syngenic mice by inhibiting the catalytic activity of CD73, and thus increasing the activity of cytotoxic T lymphocytes. In this article, we report another anticancer mechanism of anti-CD73 Abs and show that an anti-CD73 mAb (AD2) inhibits metastasis formation by a mechanism independent of CD73 catalytic activity and inhibition of primary tumor growth. This mechanism involves clustering and internalization of CD73, but does not require cross-linking of CD73, because both whole IgG anti-CD73 AD2 mAb and Fab′ fragments thereof exhibited this effect. Ex vivo treatment of different breast cancer cell lines with anti-CD73 AD2 mAb before i.v. injection into mice inhibited extravasation/colonization of circulating tumor cells and significantly reduced metastasis development. This effect was also observed when the cancer cell-surface expression of CD73 was significantly reduced by small interfering RNA knockdown. The antimetastatic activity is epitope specific, as another Ab that efficiently binds CD73-expressing live cancer cells did not lead to CD73 internalization and metastasis inhibition. Furthermore, anti-CD73 AD2 mAb inhibited development of metastasis in a spontaneous animal model of human metastatic breast cancer. Our study shows that some anti-CD73 mAbs cause cell-surface clustering of CD73 followed by internalization, thus inhibiting the ability of circulating tumor cells to extravasate and colonize, leading to inhibition of metastasis. Ab-based CD73 cancer therapy should include a combination of Abs that target the catalytic activity of CD73, as well as those with the characteristics described in this article.
      13. URL :
        http://www.jimmunol.org/content/early/2013/09/14/jimmunol.1301274.abstract
      14. Call Number :
        PKI @ catherine.lautenschlager @ 6507
      15. Serial :
        14558
      1. Author :
        Ghoneim, Hazem E.; Thomas, Paul G.; McCullers, Jonathan A.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2013
      5. Publication :
        The Journal of Immunology
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        IVIS Imaging
      12. Abstract :
        Viruses such as influenza suppress host immune function by a variety of methods. This may result in significant morbidity through several pathways, including facilitation of secondary bacterial pneumonia from pathogens such as Streptococcus pneumoniae. PKH26-phagocytic cell labeling dye was administered intranasally to label resident alveolar macrophages (AMs) in a well-established murine model before influenza infection to determine turnover kinetics during the course of infection. More than 90% of resident AMs were lost in the first week after influenza, whereas the remaining cells had a necrotic phenotype. To establish the impact of this innate immune defect, influenza-infected mice were challenged with S. pneumoniae. Early AM-mediated bacterial clearance was significantly impaired in influenza-infected mice: ∼50% of the initial bacterial inoculum could be harvested from the alveolar airspace 3 h later. In mock-infected mice, by contrast, >95% of inocula up to 50-fold higher was efficiently cleared. Coinfection during the AM depletion phase caused significant body weight loss and mortality. Two weeks after influenza, the AM population was fully replenished with successful re-establishment of early innate host protection. Local GM-CSF treatment partially restored the impaired early bacterial clearance with efficient protection against secondary pneumococcal pneumonia. We conclude that resident AM depletion occurs during influenza infection. Among other potential effects, this establishes a niche for secondary pneumococcal infection by altering early cellular innate immunity in the lungs, resulting in pneumococcal outgrowth and lethal pneumonia. This novel mechanism will inform development of novel therapeutic approaches to restore lung innate immunity against bacterial superinfections.
      13. URL :
        http://www.jimmunol.org/content/early/2013/06/26/jimmunol.1300014.abstract
      14. Call Number :
        PKI @ catherine.lautenschlager @ 5101
      15. Serial :
        14766
      1. Author :
        Albanesi, M.; Mancardi, D. A.; Macdonald, L. E.; Iannascoli, B.; Zitvogel, L.; Murphy, A. J.; Leusen, J. H.; Bruhns, P.
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2012
      5. Publication :
        J Immunol
      6. Products :
      7. Volume :
        189
      8. Issue :
        N/A
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        B16-F10-luc2, B16F10-luc2, IVIS
      12. Abstract :
        mAb therapy for experimental metastatic melanoma relies on activating receptors for the Fc portion of IgG (FcgammaR). Opposing results on the respective contribution of mouse FcgammaRI, FcgammaRIII, and FcgammaRIV have been reported using the gp75-expressing B16 melanoma and the protective anti-gp75 mAb TA99. We analyzed the contribution of FcgammaRs to this therapy model using bioluminescent measurement of lung metastases loads, novel mouse strains, and anti-FcgammaR blocking mAbs. We found that the TA99 mAb-mediated effects in a combination therapy using cyclophosphamide relied on activating FcgammaRs. The combination therapy, however, was not more efficient than mAb therapy alone. We demonstrate that FcgammaRI and, unexpectedly, FcgammaRIII contributed to TA99 mAb therapeutic effects, whereas FcgammaRIV did not. Therefore, FcgammaRIII and FcgammaRI are, together, responsible for anti-gp75 mAb therapy of B16 lung metastases. Our finding that mouse FcgammaRIII contributes to Ab-induced tumor reduction correlates with clinical data on its human functional equivalent human FcgammaRIIIA (CD16A).
      13. URL :
        http://www.ncbi.nlm.nih.gov/pubmed/23150715
      14. Call Number :
        PKI @ kd.modi @ 8
      15. Serial :
        10482
      1. Author :
        Zhang, Chenyu; Lowery, Frank J.; Yu, Dihua
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        N/A
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        120
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Cancer Research; cancer metastasis; brain metastasis; preclinical; animal model; experimental model; intracarotid injection; IVIS
      12. Abstract :
        Metastasis, the spread and growth of malignant cells at secondary sites within a patient's body, accounts for > 90% of cancer-related mortality. Recently, impressive advances in novel therapies have dramatically prolonged survival and improved quality of life for many cancer patients. Sadly, incidence of brain metastatic recurrences is fast rising, and all current therapies are merely palliative. Hence, good experimental animal models are urgently needed to facilitate in-depth studies of the disease biology and to assess novel therapeutic regimens for preclinical evaluation. However, the standard in vivo metastasis assay via tail vein injection of cancer cells produces predominantly lung metastatic lesions; animals usually succumb to the lung tumor burden before any meaningful outgrowth of brain metastasis. Intracardiac injection of tumor cells produces metastatic lesions to multiple organ sites including the brain; however, the variability of tumor growth produced with this model is large, dampening its utility in evaluating therapeutic efficacy. To generate reliable and consistent animal models for brain metastasis study, here we describe a procedure for producing experimental brain metastasis in the house mouse (Mus musculus) via intracarotid injection of tumor cells. This approach allows one to produce large number of brain metastasis-bearing mice with similar growth and mortality characteristics, thus facilitating research efforts to study basic biological mechanisms and to assess novel therapeutic agents.
      13. URL :
        https://www.jove.com/video/55085 https://www.jove.com/video/55085/intracarotid-cancer-cell-injection-to-produce-mouse-models-brain
      14. Call Number :
        PKI @ catherine.lautenschlager @ 13414
      15. Serial :
        13579
      1. Author :
        Wang, Dong; Tediashvili, Grigol; Pecha, Simon; Reichenspurner, Hermann; Deuse, Tobias; Schrepfer, Sonja
      2. Title :
      3. Type :
        Journal Article
      4. Year :
        2017
      5. Publication :
        N/A
      6. Products :
      7. Volume :
        N/A
      8. Issue :
        119
      9. Page Numbers :
        N/A
      10. Research Area :
        N/A
      11. Keywords :
        Medicine; Bypass graft failure; myointimal hyperplasia; rat model; IVIS; IVIS BLI in vivo
      12. Abstract :
        Bypass grafting is an established treatment method for coronary artery disease. Graft patency continues to be the Achilles heel of saphenous vein grafts. Research models for bypass graft failure are essential for a better understanding of pathobiological and pathophysiological processes during graft patency loss. Large animal models, such as pigs or sheep, resemble human anatomical structures but require special facilities and equipment. This video describes a rat vein interposition model to investigate vein graft patency loss. Rats are inexpensive and easy to handle. Compared to mouse models, the convenient size of rats permits better operability and enables a sufficient amount of material to be obtained for further diverse analysis. In brief, the inferior epigastric vein of a donor rat is harvested and used to replace a segment of the femoral artery. Anastomosis is conducted via single stitches and sealed with fibrin glue. Graft patency can be monitored non-invasively using duplex sonography. Myointimal hyperplasia, which is the main cause for graft patency loss, develops progressively over time and can be calculated from histological cross sections.
      13. URL :
        https://www.jove.com/video/54839 https://www.jove.com/video/54839/vein-interposition-model-suitable-model-to-study-bypass-graft
      14. Call Number :
        PKI @ catherine.lautenschlager @ 13247
      15. Serial :
        13662
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