LILRB2-mediated TREM2 signaling inhibition suppresses microglia functions

[1]  Melanie A. Huntley,et al.  Trem2 restrains the enhancement of tau accumulation and neurodegeneration by β-amyloid pathology , 2021, Neuron.

[2]  A. Mortazavi,et al.  Systematic phenotyping and characterization of the 5xFAD mouse model of Alzheimer’s disease , 2021, bioRxiv.

[3]  M. Duncan,et al.  A simple method for quantitating confocal fluorescent images , 2021, Biochemistry and biophysics reports.

[4]  Nicholas E. Propson,et al.  An epoxide hydrolase inhibitor reduces neuroinflammation in a mouse model of Alzheimer’s disease , 2020, Science Translational Medicine.

[5]  Andrew P. Hodges,et al.  Multi-omic comparison of Alzheimer’s variants in human ESC–derived microglia reveals convergence at APOE , 2020, The Journal of experimental medicine.

[6]  Qin Ma,et al.  scREAD: A Single-Cell RNA-Seq Database for Alzheimer's Disease , 2020, bioRxiv.

[7]  D. Walker Defining activation states of microglia in human brain tissue: an unresolved issue for Alzheimer’s disease , 2020 .

[8]  H. Rhinn,et al.  Anti-human TREM2 induces microglia proliferation and reduces pathology in an Alzheimer’s disease model , 2020, The Journal of experimental medicine.

[9]  Terrance T. Kummer,et al.  Impact of TREM2R47H variant on tau pathology-induced gliosis and neurodegeneration. , 2020, The Journal of clinical investigation.

[10]  M. Simons,et al.  Enhancing protective microglial activities with a dual function TREM2 antibody to the stalk region , 2020, EMBO molecular medicine.

[11]  L. Schneider,et al.  The clinical promise of biomarkers of synapse damage or loss in Alzheimer’s disease , 2020, Alzheimer's Research & Therapy.

[12]  R. Jaenisch,et al.  Human iPSC-derived microglia assume a primary microglia-like state after transplantation into the neonatal mouse brain , 2019, Proceedings of the National Academy of Sciences.

[13]  J. Elmquist,et al.  Partial Leptin Reduction as an Insulin Sensitization and Weight Loss Strategy. , 2019, Cell metabolism.

[14]  D. Holtzman,et al.  Alzheimer Disease: An Update on Pathobiology and Treatment Strategies , 2019, Cell.

[15]  R. Tanzi,et al.  TREM2 Acts Downstream of CD33 in Modulating Microglial Pathology in Alzheimer’s Disease , 2019, Neuron.

[16]  Anne-Laure Hemonnot,et al.  Microglia in Alzheimer Disease: Well-Known Targets and New Opportunities , 2019, Front. Aging Neurosci..

[17]  N. V. van Nuland,et al.  Apolipoprotein E associated with reconstituted high‐density lipoprotein‐like particles is protected from aggregation , 2019, FEBS letters.

[18]  M. Colonna,et al.  Aminophospholipids are signal-transducing TREM2 ligands on apoptotic cells , 2019, Scientific Reports.

[19]  Huaxi Xu,et al.  Soluble TREM2 ameliorates pathological phenotypes by modulating microglial functions in an Alzheimer’s disease model , 2019, Nature Communications.

[20]  S. Strittmatter,et al.  Systematic and standardized comparison of reported amyloid-β receptors for sufficiency, affinity, and Alzheimer's disease relevance , 2019, The Journal of Biological Chemistry.

[21]  M. Aglietta,et al.  NK-mediated antibody-dependent cell-mediated cytotoxicity in solid tumors: biological evidence and clinical perspectives. , 2019, Annals of translational medicine.

[22]  D. Holtzman,et al.  New insights into the role of TREM2 in Alzheimer’s disease , 2018, Molecular Neurodegeneration.

[23]  Sathish Kumar Mungamuri,et al.  Blocking immunoinhibitory receptor LILRB2 reprograms tumor-associated myeloid cells and promotes antitumor immunity , 2018, The Journal of clinical investigation.

[24]  D. Black,et al.  Inhibiting Amyloid-ß cytotoxicity through its interaction with the cell surface receptor LilrB2 by structure-based design , 2018, Nature Chemistry.

[25]  M. Colonna,et al.  TREM2 — a key player in microglial biology and Alzheimer disease , 2018, Nature Reviews Neurology.

[26]  D. Holtzman,et al.  Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight , 2018, Nature Reviews Immunology.

[27]  I. Amit,et al.  Disease-Associated Microglia: A Universal Immune Sensor of Neurodegeneration , 2018, Cell.

[28]  Huaxi Xu,et al.  Amyloid-beta modulates microglial responses by binding to the triggering receptor expressed on myeloid cells 2 (TREM2) , 2018, Molecular Neurodegeneration.

[29]  Huaxi Xu,et al.  TREM2 Is a Receptor for β-Amyloid that Mediates Microglial Function , 2018, Neuron.

[30]  B. Barres,et al.  Microglia and macrophages in brain homeostasis and disease , 2017, Nature Reviews Immunology.

[31]  C. Brayne,et al.  TREM2 expression in the human brain: a marker of monocyte recruitment? , 2017, Brain pathology.

[32]  C. V. van Dyck Anti-Amyloid-β Monoclonal Antibodies for Alzheimer’s Disease: Pitfalls and Promise , 2017, Biological Psychiatry.

[33]  R. Ransohoff,et al.  TREM2 deficiency exacerbates tau pathology through dysregulated kinase signaling in a mouse model of tauopathy , 2017, Molecular Neurodegeneration.

[34]  D. Holtzman,et al.  TREM2 deficiency attenuates neuroinflammation and protects against neurodegeneration in a mouse model of tauopathy , 2017, Proceedings of the National Academy of Sciences.

[35]  Markus Glatzel,et al.  The TREM2-APOE Pathway Drives the Transcriptional Phenotype of Dysfunctional Microglia in Neurodegenerative Diseases. , 2017, Immunity.

[36]  Maxim N. Artyomov,et al.  TREM2 Maintains Microglial Metabolic Fitness in Alzheimer’s Disease , 2017, Cell.

[37]  W. Wurst,et al.  The FTD‐like syndrome causing TREM2 T66M mutation impairs microglia function, brain perfusion, and glucose metabolism , 2017, The EMBO journal.

[38]  Michael D. Cahalan,et al.  iPSC-Derived Human Microglia-like Cells to Study Neurological Diseases , 2017, Neuron.

[39]  R. Tanzi,et al.  Alzheimer's disease-associated TREM2 variants exhibit either decreased or increased ligand-dependent activation , 2017, Alzheimer's & Dementia.

[40]  D. Maric,et al.  Differentiation of human and murine induced pluripotent stem cells to microglia-like cells , 2017, Nature Neuroscience.

[41]  D. Kober,et al.  Triggering receptor expressed on myeloid cells 2 , 2016 .

[42]  Chan-Sik Park,et al.  Immunohistochemistry for Pathologists: Protocols, Pitfalls, and Tips , 2016, Journal of pathology and translational medicine.

[43]  Lino C. Gonzalez,et al.  TREM2 Binds to Apolipoproteins, Including APOE and CLU/APOJ, and Thereby Facilitates Uptake of Amyloid-Beta by Microglia , 2016, Neuron.

[44]  D. Holtzman,et al.  TREM2-mediated early microglial response limits diffusion and toxicity of amyloid plaques , 2016, The Journal of experimental medicine.

[45]  U. Sengupta,et al.  The Role of Amyloid-β Oligomers in Toxicity, Propagation, and Immunotherapy , 2016, EBioMedicine.

[46]  R. Birge,et al.  Phosphatidylserine is a global immunosuppressive signal in efferocytosis, infectious disease, and cancer , 2016, Cell Death and Differentiation.

[47]  J. Cambier,et al.  Of ITIMs, ITAMs, and ITAMis: revisiting immunoglobulin Fc receptor signaling , 2015, Immunological reviews.

[48]  S. Paul,et al.  Microglial internalization and degradation of pathological tau is enhanced by an anti-tau monoclonal antibody , 2015, Scientific Reports.

[49]  S. Ferreira,et al.  Soluble amyloid-β oligomers as synaptotoxins leading to cognitive impairment in Alzheimer’s disease , 2015, Front. Cell. Neurosci..

[50]  Anil Kumar,et al.  A review on Alzheimer’s disease pathophysiology and its management: an update , 2015, Pharmacological reports : PR.

[51]  P. Séguéla,et al.  P2Y12 expression and function in alternatively activated human microglia , 2015, Neurology: Neuroimmunology & Neuroinflammation.

[52]  R. Ransohoff,et al.  TREM2 deficiency eliminates TREM2+ inflammatory macrophages and ameliorates pathology in Alzheimer’s disease mouse models , 2015, The Journal of experimental medicine.

[53]  D. Holtzman,et al.  TREM2 lipid sensing sustains microglia response in an Alzheimer’s disease model , 2015, Cell.

[54]  R. Wilkinson,et al.  The role of Fc gamma receptors in the activity of immunomodulatory antibodies for cancer , 2014, Journal of Immunotherapy for Cancer.

[55]  G. Gao,et al.  A motif in LILRB2 critical for Angptl2 binding and activation. , 2014, Blood.

[56]  J. Molinuevo,et al.  TREM2 mutations implicated in neurodegeneration impair cell surface transport and phagocytosis , 2014, Science Translational Medicine.

[57]  Xavier Robert,et al.  Deciphering key features in protein structures with the new ENDscript server , 2014, Nucleic Acids Res..

[58]  J. Coligan,et al.  p85α recruitment by the CD300f phosphatidylserine receptor mediates apoptotic cell clearance required for autoimmunity suppression , 2014, Nature Communications.

[59]  M. Staufenbiel,et al.  Membrane-Anchored Aβ Accelerates Amyloid Formation and Exacerbates Amyloid-Associated Toxicity in Mice , 2013, The Journal of Neuroscience.

[60]  Bradley T. Hyman,et al.  Human LilrB2 Is a β-Amyloid Receptor and Its Murine Homolog PirB Regulates Synaptic Plasticity in an Alzheimer’s Model , 2013, Science.

[61]  Bradley T. Hyman,et al.  Alzheimer’s Disease Risk Gene CD33 Inhibits Microglial Uptake of Amyloid Beta , 2013, Neuron.

[62]  Xue-jun Fan,et al.  HER3 intracellular domains play a crucial role in HER3/HER2 dimerization and activation of downstream signaling pathways , 2012, Protein & Cell.

[63]  M. Masserini,et al.  Binding of β-amyloid (1-42) peptide to negatively charged phospholipid membranes in the liquid-ordered state: modeling and experimental studies. , 2012, Biophysical journal.

[64]  K. Ohashi,et al.  Cytochalasin D acts as an inhibitor of the actin-cofilin interaction. , 2012, Biochemical and biophysical research communications.

[65]  Xue-jun Fan,et al.  ERBB3 (HER3) is a key sensor in the regulation of ERBB-mediated signaling in both low and high ERBB2 (HER2) expressing cancer cells , 2012, Cancer medicine.

[66]  K. Hensley,et al.  A comparative review of cell culture systems for the study of microglial biology in Alzheimer’s disease , 2012, Journal of Neuroinflammation.

[67]  J. Andersen,et al.  Human CD300a binds to phosphatidylethanolamine and phosphatidylserine, and modulates the phagocytosis of dead cells. , 2012, Blood.

[68]  J. McLaurin,et al.  Clearance of amyloid-β peptides by microglia and macrophages: the issue of what, when and where. , 2012, Future neurology.

[69]  H. Nakanishi,et al.  Phosphatidylserine-containing liposomes suppress inflammatory bone loss by ameliorating the cytokine imbalance provoked by infiltrated macrophages , 2011, Laboratory Investigation.

[70]  A. Sheikh,et al.  Lysophosphatidylcholine modulates fibril formation of amyloid beta peptide , 2011, The FEBS journal.

[71]  Fei Liu,et al.  Tau in Alzheimer disease and related tauopathies. , 2010, Current Alzheimer research.

[72]  C. Reutelingsperger,et al.  Phosphatidylserine targeting for diagnosis and treatment of human diseases , 2010, Apoptosis.

[73]  T. Bayer,et al.  Formic acid is essential for immunohistochemical detection of aggregated intraneuronal Aβ peptides in mouse models of Alzheimer's disease , 2009, Brain Research.

[74]  Denise C. Park,et al.  Beta-Amyloid Deposition and the Aging Brain , 2009, Neuropsychology Review.

[75]  W. Seaman,et al.  A role for TREM2 ligands in the phagocytosis of apoptotic neuronal cells by microglia , 2009, Journal of neurochemistry.

[76]  Khadija Iqbal,et al.  Hyperphosphorylation of microtubule-associated protein tau: a promising therapeutic target for Alzheimer disease. , 2008, Current medicinal chemistry.

[77]  A. Kraft,et al.  Neuroinflammation and microglia: considerations and approaches for neurotoxicity assessment , 2008, Expert opinion on drug metabolism & toxicology.

[78]  L. Lanier,et al.  Cutting Edge: Inhibition of TLR and FcR Responses in Macrophages by Triggering Receptor Expressed on Myeloid Cells (TREM)-2 and DAP121 , 2006, The Journal of Immunology.

[79]  R. Birge,et al.  Phosphatidylserine recognition by phagocytes: a view to a kill. , 2006, Trends in cell biology.

[80]  Hirohisa Tajima,et al.  Neuronal cell death in Alzheimer's disease and a neuroprotective factor, humanin. , 2006, Current neuropharmacology.

[81]  C. June,et al.  SHP-1 and SHP-2 Associate with Immunoreceptor Tyrosine-Based Switch Motif of Programmed Death 1 upon Primary Human T Cell Stimulation, but Only Receptor Ligation Prevents T Cell Activation1 , 2004, The Journal of Immunology.

[82]  Takashi Saito,et al.  NFAM1, an immunoreceptor tyrosine-based activation motif-bearing molecule that regulates B cell development and signaling. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[83]  A. West,et al.  Crystal structure of LIR-2 (ILT4) at 1.8 Å: differences from LIR-1 (ILT2) in regions implicated in the binding of the Human Cytomegalovirus class I MHC homolog UL18 , 2002, BMC Structural Biology.

[84]  L. Lanier,et al.  Direct Recognition of Cytomegalovirus by Activating and Inhibitory NK Cell Receptors , 2002, Science.

[85]  P. Leibson,et al.  ITAMs versus ITIMs: striking a balance during cell regulation. , 2002, The Journal of clinical investigation.

[86]  G. Ogg,et al.  Human myelomonocytic cells express an inhibitory receptor for classical and nonclassical MHC class I molecules. , 1998, Journal of immunology.

[87]  J. Henzen Publisher's note , 1979, Brain Research.