@article{67b1ab3a8b41405d84fa79a9457c5771,
title = "Neutrophil derived CSF1 induces macrophage polarization and promotes transplantation tolerance",
abstract = "The colony-stimulating factor 1 (CSF1) regulates the differentiation and function of tissue macrophages and determines the outcome of the immune response. The molecular mechanisms behind CSF1-mediated macrophage development remain to be elucidated. Here we demonstrate that neutrophil-derived CSF1 controls macrophage polarization and proliferation, which is necessary for the induction of tolerance. Inhibiting neutrophil production of CSF1 or preventing macrophage proliferation, using targeted nanoparticles loaded with the cell cycle inhibitor simvastatin, abrogates the induction of tolerance. These results provide new mechanistic insights into the developmental requirements of tolerogenic macrophages and identify CSF1 producing neutrophils as critical regulators of the immunological response.",
keywords = "basic (laboratory) research/science, immunobiology, macrophage/monocyte biology: differentiation/maturation, tolerance: mechanisms",
author = "Braza, {Mounia S.} and Patricia Conde and Mercedes Garcia and Isabel Cortegano and Manisha Brahmachary and Venu Pothula and Francois Fay and Peter Boros and Werner, {Sherry A.} and Florent Ginhoux and Mulder, {Willem J.M.} and Jordi Ochando",
note = "Funding Information: We thank the technical contributions of the flow cytometry and microsurgery cores at Mount Sinai. We also acknowledge Marcy Kuenzel and Sridar Chittur at the University of Albany Center for Functional Genomics microarray core facility for their assistance in generating the microarray data. This work was supported by the Cancer Center Grant P30 CA196521; the National Institute of Health grants AG045040 to S.A.W. and R01 HL118440, R01 HL125703, R01 CA155432 to W.J.M.M; and the Ministerio de Economia y Competitividad SAF2016-80031-R to J.O. This work was also supported by the COST Action BM1305: Action to Focus and Accelerate Cell Tolerogenic Therapies (A FACTT), the COST action BM1404: European Network of Investigators Triggering Exploratory Research on Myeloid Regulatory Cells (Mye-EUNITER), Funding Information: We thank the technical contributions of the flow cytometry and microsurgery cores at Mount Sinai. We also acknowledge Marcy Kuenzel and Sridar Chittur at the University of Albany Center for Functional Genomics microarray core facility for their assistance in generating the microarray data. This work was supported by the Cancer Center Grant P30 CA196521; the National Institute of Health grants AG045040 to S.A.W. and R01 HL118440, R01 HL125703, R01 CA155432 to W.J.M.M; and the Ministerio de Economia y Competitividad SAF2016-80031-R to J.O. This work was also supported by the COST Action BM1305: Action to Focus and Accelerate Cell Tolerogenic Therapies (A?FACTT), the COST action BM1404: European Network of Investigators Triggering Exploratory Research on Myeloid Regulatory Cells (Mye-EUNITER), and the Mount Sinai Recanati/Miller Transplantation Institute career development funds. Publisher Copyright: {\textcopyright} 2018 The Authors. American Journal of Transplantation published by Wiley Periodicals, Inc. on behalf of The American Society of Transplantation and the American Society of Transplant Surgeons",
year = "2018",
month = may,
doi = "10.1111/ajt.14645",
language = "English (US)",
volume = "18",
pages = "1247--1255",
journal = "American Journal of Transplantation",
issn = "1600-6135",
publisher = "Wiley-Blackwell",
number = "5",
}