@article{HaakeHaackSchaeferetal.2023,
  author    = {Haake, Markus and Haack, Beatrice and Sch{\"a}fer, Tina and Harter, Patrick N. and Mattavelli, Greta and Eiring, Patrick and Vashist, Neha and Wedekink, Florian and Genssler, Sabrina and Fischer, Birgitt and Dahlhoff, Julia and Mokhtari, Fatemeh and Kuzkina, Anastasia and Welters, Marij J. P. and Benz, Tamara M. and Sorger, Lena and Thiemann, Vincent and Almanzar, Giovanni and Selle, Martina and Thein, Klara and Sp{\"a}th, Jacob and Gonzalez, Maria Cecilia and Reitinger, Carmen and Ipsen-Escobedo, Andrea and Wistuba-Hamprecht, Kilian and Eichler, Kristin and Filipski, Katharina and Zeiner, Pia S. and Beschorner, Rudi and Goedemans, Renske and Gogolla, Falk Hagen and Hackl, Hubert and Rooswinkel, Rogier W. and Thiem, Alexander and Romer Roche, Paula and Joshi, Hemant and P{\"u}hringer, Dirk and W{\"o}ckel, Achim and Diessner, Joachim E. and R{\"u}diger, Manfred and Leo, Eugen and Cheng, Phil F. and Levesque, Mitchell P. and Goebeler, Matthias and Sauer, Markus and Nimmerjahn, Falk and Schuberth-Wagner, Christine and Felten, Stefanie von and Mittelbronn, Michel and Mehling, Matthias and Beilhack, Andreas and van der Burg, Sjoerd H. and Riedel, Angela and Weide, Benjamin and Dummer, Reinhard and Wischhusen, J{\"o}rg},
  title     = {Tumor-derived GDF-15 blocks LFA-1 dependent T cell recruitment and suppresses responses to anti-PD-1 treatment},
  series = {Nature Communications},
  volume    = {14},
  journal   = {Nature Communications},
  doi       = {10.1038/s41467-023-39817-3},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-357333},
  year      = {2023},
  abstract  = {Immune checkpoint blockade therapy is beneficial and even curative for some cancer patients. However, the majority don't respond to immune therapy. Across different tumor types, pre-existing T cell infiltrates predict response to checkpoint-based immunotherapy. Based on in vitro pharmacological studies, mouse models and analyses of human melanoma patients, we show that the cytokine GDF-15 impairs LFA-1/β2-integrin-mediated adhesion of T cells to activated endothelial cells, which is a pre-requisite of T cell extravasation. In melanoma patients, GDF-15 serum levels strongly correlate with failure of PD-1-based immune checkpoint blockade therapy. Neutralization of GDF-15 improves both T cell trafficking and therapy efficiency in murine tumor models. Thus GDF-15, beside its known role in cancer-related anorexia and cachexia, emerges as a regulator of T cell extravasation into the tumor microenvironment, which provides an even stronger rationale for therapeutic anti-GDF-15 antibody development.},
  language  = {en}
}
@article{PellegrinoDelBufaloDeAngelisetal.2020,
  author    = {Pellegrino, Marsha and Del Bufalo, Francesca and De Angelis, Biagio and Quintarelli, Concetta and Caruana, Ignazio and de Billy, Emmanuel},
  title     = {Manipulating the metabolism to improve the efficacy of CAR T-cell immunotherapy},
  series = {Cells},
  volume    = {10},
  journal   = {Cells},
  number    = {1},
  issn      = {2073-4409},
  doi       = {10.3390/cells10010014},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-220140},
  year      = {2020},
  abstract  = {The adoptive transfer of the chimeric antigen receptor (CAR) expressing T-cells has produced unprecedented successful results in the treatment of B-cell malignancies. However, the use of this technology in other malignancies remains less effective. In the setting of solid neoplasms, CAR T-cell metabolic fitness needs to be optimal to reach the tumor and execute their cytolytic function in an environment often hostile. It is now well established that both tumor and T cell metabolisms play critical roles in controlling the immune response by conditioning the tumor microenvironment and the fate and activity of the T cells. In this review, after a brief description of the tumoral and T cell metabolic reprogramming, we summarize the latest advances and new strategies that have been developed to improve the metabolic fitness and efficacy of CAR T-cell products.},
  language  = {en}
}
@article{EyrichRachorSchreiberetal.2013,
  author    = {Eyrich, Matthias and Rachor, Johannes and Schreiber, Susanne C. and W{\"o}lfl, Matthias and Schlegel, Paul G.},
  title     = {Dendritic cell vaccination in pediatric gliomas: lessons learnt and future perspectives},
  series = {Frontiers in Pediatrics},
  journal   = {Frontiers in Pediatrics},
  doi       = {10.3389/fped.2013.00012},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-96937},
  year      = {2013},
  abstract  = {Immunotherapy of malignant gliomas with autologous dendritic cells (DCs) in addition to surgery and radiochemotherapy has been a focus of intense research during the past decade. Since both children and adults are affected by this highly aggressive brain tumor, 10-15\% of the several hundred vaccinated patients represent children, making pediatric glioma patients the largest uniform pediatric vaccination cohort so far. In general, DC vaccination in malignant gliomas has been shown to be safe and several studies with a non-vaccinated control group could clearly demonstrate a survival benefit for the vaccinated patients. Interestingly, children and adolescents below 21 years of age seem to benefit even more than adult patients. This review summarizes the findings of the 25 clinical trials published so far and gives a perspective how DC vaccination could be implemented as part of multimodal therapeutic strategies in the near future.},
  language  = {en}
}
@article{SchilbachAlkhaledWelkeretal.2015,
  author    = {Schilbach, Karin and Alkhaled, Mohammed and Welker, Christian and Eckert, Franziska and Blank, Gregor and Ziegler, Hendrik and Sterk, Marco and M{\"u}ller, Friederike and Sonntag, Katja and Wieder, Thomas and Braum{\"u}ller, Heidi and Schmitt, Julia and Eyrich, Matthias and Schleicher, Sabine and Seitz, Christian and Erbacher, Annika and Pichler, Bernd J. and M{\"u}ller, Hartmut and Tighe, Robert and Lim, Annick and Gillies, Stephen D. and Strittmatter, Wolfgang and R{\"o}cken, Martin and Handgretinger, Rupert},
  title     = {Cancer-targeted IL-12 controls human rhabdomyosarcoma by senescence induction and myogenic differentiation},
  series = {OncoImmunology},
  volume    = {4},
  journal   = {OncoImmunology},
  number    = {7},
  doi       = {10.1080/2162402X.2015.1014760},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-154579},
  pages     = {e1014760},
  year      = {2015},
  abstract  = {Stimulating the immune system to attack cancer is a promising approach, even for the control of advanced cancers. Several cytokines that promote interferon-γ-dominated immune responses show antitumor activity, with interleukin 12 (IL-12) being of major importance. Here, we used an antibody-IL-12 fusion protein (NHS-IL12) that binds histones of necrotic cells to treat human sarcoma in humanized mice. Following sarcoma engraftment, NHS-IL12 therapy was combined with either engineered IL-7 (FcIL-7) or IL-2 (IL-2MAB602) for continuous cytokine bioavailability. NHS-IL12 strongly induced innate and adaptive antitumor immunity when combined with IL-7 or IL-2. NHS-IL12 therapy significantly improved survival of sarcoma-bearing mice and caused long-term remissions when combined with IL-2. NHS-IL12 induced pronounced cancer cell senescence, as documented by strong expression of senescence-associated p16\(^{INK4a}\) and nuclear translocation of p-HP1γ, and permanent arrest of cancer cell proliferation. In addition, this cancer immunotherapy initiated the induction of myogenic differentiation, further promoting the hypothesis that efficient antitumor immunity includes mechanisms different from cytotoxicity for efficient cancer control in vivo.},
  language  = {en}
}