Research Topics
Genomes and Genes
Species | Terrence TownSummaryAffiliation: Cedars-Sinai Medical Center Country: USA Publications
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Detail Information
Publications
Reduced Th1 and enhanced Th2 immunity after immunization with Alzheimer's beta-amyloid(1-42)Terrence Town
Roskamp Institute, University of South Florida, 3515 E Fletcher Avenue, Tampa, FL 33613, USA
J Neuroimmunol 132:49-59. 2002..Taken together, these results show enhanced Th2 and down-regulated Th1 immunity following immune challenge with Abeta(1-42)...- CD40 signaling regulates innate and adaptive activation of microglia in response to amyloid beta-peptideKirk P Townsend
Neuroimmunology Laboratory, Department of Psychiatry, University of South Florida College of Medicine, Tampa, USA
Eur J Immunol 35:901-10. 2005..These data provide a mechanistic explanation for our previous work showing decreased microgliosis associated with diminished cerebral Abeta/beta-amyloid pathology when blocking CD40 signaling in transgenic Alzheimer's mice... - Green tea epigallocatechin-3-gallate (EGCG) modulates amyloid precursor protein cleavage and reduces cerebral amyloidosis in Alzheimer transgenic miceKavon Rezai-Zadeh
Silver Child Development Center, Department of Psychiatry and Behavioral Medicine, University of South Florida, Tampa, Florida 33613, USA
J Neurosci 25:8807-14. 2005..These data raise the possibility that EGCG dietary supplementation may provide effective prophylaxis for AD... - West Nile virus envelope protein inhibits dsRNA-induced innate immune responsesAlvaro Arjona
Section of Infectious Diseases, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA
J Immunol 179:8403-9. 2007..In conclusion, these data show that the major structural protein of WNV impairs the innate immune response and suggest that WNV exploits differential vector/host E glycosylation profiles to evade antiviral mechanisms... 
Inflammaging as a prodrome to Alzheimer's diseaseBrian Giunta
Neuroimmunology Laboratory, Department of Psychiatry, Behavioral Medicine, Institute for Research in Psychiatry, University of South Florida, College of Medicine, Tampa, FL 33613, USA
J Neuroinflammation 5:51. 2008..In addition, we explain how three novel treatments, (1) human umbilical cord blood cells (HUCBC), (2) flavanoids, and (3) Abeta vaccination oppose the forces of inflammaging and AD-like pathology in various mouse models...- Alternative Abeta immunotherapy approaches for Alzheimer's diseaseTerrence Town
Department of Neurosurgery, Maxine Dunitz Neurosurgical Institute, Cedars Sinai Medical Center, Los Angeles, CA 90048, USA
CNS Neurol Disord Drug Targets 8:114-27. 2009..Specifically, the focus is on those strategies that target inflammatory and immune aspects of AD, and can therefore be classified as immunotherapeutic in a broad sense... - Blocking TGF-beta-Smad2/3 innate immune signaling mitigates Alzheimer-like pathologyTerrence Town
Department of Immunobiology, Yale University School of Medicine, 300 Cedar Street, New Haven, Connecticut 06520 8011, USA
Nat Med 14:681-7. 2008..Taken together, our results suggest that blockade of TGF-beta-Smad2/3 signaling in peripheral macrophages represents a new therapeutic target for Alzheimer's disease... - Alzheimer's Disease Beyond AbetaTerrence Town
Department of Biomedical Sciences, Regenerative Medicine Institute, Cedars Sinai Medical Center, SSB3 Room 361, Los Angeles, CA 90048, USA
Expert Rev Neurother 10:671-5. 2010..Despite illuminating scientific presentations and intense discussions, a number of important questions remain concerning the best biomarkers and targets to focus on, and when and how to therapeutically intervene... - Toll-like receptor 7 mitigates lethal West Nile encephalitis via interleukin 23-dependent immune cell infiltration and homingTerrence Town
Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
Immunity 30:242-53. 2009..Collectively, these results demonstrate that TLR7 and IL-23-dependent WNV responses represent a vital host defense mechanism that operates by affecting immune cell homing to infected target cells... - IL-10 signaling blockade controls murine West Nile virus infectionFengwei Bai
Section of Infectious Diseases, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, United States of America
PLoS Pathog 5:e1000610. 2009..In conclusion, IL-10 signaling plays a negative role in immunity against WNV infection, and blockade of IL-10 signaling by genetic or pharmacologic means helps to control viral infection, suggesting a novel anti-WNV therapeutic strategy... - IL-22 signaling contributes to West Nile encephalitis pathogenesisPenghua Wang
Section of Infectious Diseases, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA
PLoS ONE 7:e44153. 2012..Our results suggest that IL-22 signaling exacerbates lethal WNV encephalitis likely by promoting WNV neuroinvasion... - A protective function for interleukin 17A in T cell-mediated intestinal inflammationWilliam O'Connor
Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut, USA
Nat Immunol 10:603-9. 2009..Our data demonstrate a protective function for IL-17 and identify T cells as not only the source but also a target of IL-17 in vivo... - Adaptive and innate transforming growth factor beta signaling impact herpes simplex virus 1 latency and reactivationSariah J Allen
Center for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery and Regenerative Medicine Institute, Los Angeles, California 90048, USA
J Virol 85:11448-56. 2011..These findings strongly suggest that TGF-β signaling, which generally functions to dampen immune responses, results in increased HSV-1 latency... - TGF-beta signaling in dendritic cells is a prerequisite for the control of autoimmune encephalomyelitisYasmina Laouar
Department of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
Proc Natl Acad Sci U S A 105:10865-70. 2008..Our data provide direct evidence that TGF-beta can control autoimmunity via actions on DCs... - Microglia recognize double-stranded RNA via TLR3Terrence Town
Section of Immunobiology, Yale University School of Medicine, 300 Cedar Street, New Haven, CT 06520, USA
J Immunol 176:3804-12. 2006..When taken together, our results demonstrate that microglia recognize dsRNA through TLR3 and associated signaling molecules and suggest that these cells are key sensors of dsRNA-producing viruses that may invade the CNS... - Control of TH17 cells occurs in the small intestineEnric Esplugues
Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
Nature 475:514-8. 2011..These results identify mechanisms limiting T(H)17 cell pathogenicity and implicate the gastrointestinal tract as a site for control of T(H)17 cells... - Macrophage IL-12p70 signaling prevents HSV-1-induced CNS autoimmunity triggered by autoaggressive CD4+ TregsKevin R Mott
Center for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery and Regenerative Medicine Institute, Cedars Sinai Medical Center, Los Angeles, California, USA
Invest Ophthalmol Vis Sci 52:2321-33. 2011..However, it is unclear whether innate immune cells modulate Treg function. Here the authors examined the role of innate immunity in lymphomyeloid homeostasis... - Icam-1 participates in the entry of west nile virus into the central nervous systemJianfeng Dai
Section of Infectious Diseases, Department of Internal Medicine, Yale University School of Medicine, P O Box 208031, New Haven, CT 06520 8031, USA
J Virol 82:4164-8. 2008..These data suggest that ICAM-1 plays an important role in West Nile virus neuroinvasion and that targeting ICAM-1 signaling may help control viral encephalitis... - Rapid genetic targeting of pial surface neural progenitors and immature neurons by neonatal electroporationJoshua J Breunig
Regenerative Medicine Institute, SSB 345, Los Angeles, CA 90048, USA
Neural Dev 7:26. 2012..However, their contribution to the histogenesis of the cortex remains poorly understood due to difficulties associated with genetically manipulating these unique cells in a population-specific manner... - The role of LAT in increased CD8+ T cell exhaustion in trigeminal ganglia of mice latently infected with herpes simplex virus 1Sariah J Allen
Center for Neurobiology and Vaccine Development, D2024, Cedars Sinai Burns and Allen Research Institute, 8700 Beverly Blvd, Los Angeles, CA 90048, USA
J Virol 85:4184-97. 2011..Together, these results may suggest that both PD-1 and Tim-3 are mediators of CD8(+) T cell exhaustion and latency in HSV-1 infection... - Toll-like receptor modulation of murine cerebral malaria is dependent on the genetic background of the hostJason W Griffith
Department of Internal Medicine, Yale University, 300 Cedar Street, New Haven, CT 06520, USA
J Infect Dis 196:1553-64. 2007..These results suggest that TLR signaling and host genetic background influences the pathogenesis of CM via modulation of cytokine production and T(reg) cell numbers... - Macrophages in Alzheimer's disease: the blood-borne identityDavid Gate
Department of Biomedical Sciences, Regenerative Medicine Institute, Cedars Sinai Medical Center, 8700 Beverly Blvd, Steven Spielberg Building, Room 361, Los Angeles, CA 90048, USA
J Neural Transm 117:961-70. 2010.... - CNS infiltration of peripheral immune cells: D-Day for neurodegenerative disease?Kavon Rezai-Zadeh
Department of Biomedical Sciences, Cedars Sinai Medical Center, Los Angeles, CA 90048, USA
J Neuroimmune Pharmacol 4:462-75. 2009.... - Abrogation of macrophage migration inhibitory factor decreases West Nile virus lethality by limiting viral neuroinvasionAlvaro Arjona
Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut, USA
J Clin Invest 117:3059-66. 2007.... - T-cells in Alzheimer's diseaseTerrence Town
Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA
Neuromolecular Med 7:255-64. 2005..Finally, we explore the use of mouse models of AD as a system within which to definitively test the possible contribution of T-cells to AD pathogenesis... 
Basic biology and mechanisms of neural ciliogenesis and the B9 familyDavid Gate
Department of Biomedical Sciences and Regenerative Medicine Institute, Cedars Sinai Medical Center, Los Angeles, CA 90048, USA
Mol Neurobiol 45:564-70. 2012..When taken together, the studies reviewed herein point to critical roles played by neural cilia, both in normal physiology and in disease...- Oxidized mitochondrial DNA activates the NLRP3 inflammasome during apoptosisKenichi Shimada
Division of Pediatrics Infectious Disease and Immunology, Cedars Sinai Medical Center and David Geffen School of Medicine, UCLA, Los Angeles, CA 90048, USA
Immunity 36:401-14. 2012..These results provide a missing link between apoptosis and inflammasome activation, via binding of cytosolic oxidized mtDNA to the NLRP3 inflammasome... - Can peripheral leukocytes be used as Alzheimer's disease biomarkers?Kavon Rezai-Zadeh
Department of Biomedical Sciences, Cedars Sinai Medical Center, Los Angeles, CA 90048, USA
Expert Rev Neurother 9:1623-33. 2009..In this review, we critically analyze the potential utility of peripheral leukocytes as biological markers for AD... - A role for the JAK-STAT1 pathway in blocking replication of HSV-1 in dendritic cells and macrophagesKevin R Mott
Center for Neurobiology and Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars Sinai Medical Center, Los Angeles, CA, USA
Virol J 6:56. 2009..The aim of our study was to determine factor (s) that are involved in the resistance of DCs and macrophages to productive HSV-1 infection... - Antiviral peptides targeting the west nile virus envelope proteinFengwei Bai
Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA
J Virol 81:2047-55. 2007..These short peptides serve as the basis for developing new therapeutics for West Nile encephalitis and, potentially, other flaviviruses... - Defective p53 engagement after the induction of DNA damage in cells deficient in topoisomerase 3betaSubhasis Mohanty
Section of Infectious Diseases, Departments of Internal Medicine and Immunobiology, Yale University School of Medicine, New Haven, CT 06520
Proc Natl Acad Sci U S A 105:5063-8. 2008..Taken together, these results suggest an unanticipated role for Top3beta beyond DNA repair in the activation of cellular responses to DNA damage... - Myeloid differentiation factor-2 interacts with Lyn kinase and is tyrosine phosphorylated following lipopolysaccharide-induced activation of the TLR4 signaling pathwayPearl Gray
Division of Pediatric Infectious Diseases and Immunology, Cedars Sinai Medical Center, Los Angeles, CA 90048, USA
J Immunol 187:4331-7. 2011..Our study demonstrated that tyrosine phosphorylation of MD-2 is important for signaling following exposure to LPS and underscores the importance of this event in mediating an efficient and prompt immune response... - Interchromosomal associations between alternatively expressed lociCharalampos G Spilianakis
Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA
Nature 435:637-45. 2005..Thus, we provide an example of eukaryotic genes located on separate chromosomes associating physically in the nucleus via interactions that may have a function in coordinating gene expression... - Apoptotic hepatocyte DNA inhibits hepatic stellate cell chemotaxis via toll-like receptor 9Azuma Watanabe
Section of Digestive Diseases, Yale University School of Medicine, New Haven, CT, USA
Hepatology 46:1509-18. 2007.... - Toll-like receptor 3 mediates West Nile virus entry into the brain causing lethal encephalitisTian Wang
Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, 300 Cedar Street, New Haven, Connecticut 06520, USA
Nat Med 10:1366-73. 2004..Collectively, WNV infection leads to a Tlr3-dependent inflammatory response, which is involved in brain penetration of the virus and neuronal injury... - The stumpy gene is required for mammalian ciliogenesisTerrence Town
Department of Immunobiology and Neurobiology, Section of Nephrology, Yale University School of Medicine, 300 Cedar Street, TAC S 569, New Haven, CT 06519 8011, USA
Proc Natl Acad Sci U S A 105:2853-8. 2008..Therefore, stumpy is essential for ciliogenesis and may be involved in the pathogenesis of human congenital malformations such as HC and PKD... - Behavioral effects of CD40-CD40L pathway disruption in aged PSAPP miceJ Todd Roach
Roskamp Institute, 2040 Whitfield Avenue, Sarasota, FL 34243, USA
Brain Res 1015:161-8. 2004..Disruption of CD40L activity has beneficial effects on pathology and cognitive behavior in the PSAPP mouse model, providing support for the therapeutic potential of interrupting the CD40-CD40L interaction in AD... - CD45 isoform alteration in CD4+ T cells as a potential diagnostic marker of Alzheimer's diseaseJun Tan
Department of Psychiatry, Roskamp Institute, University of South Florida, 3515 E Fletcher Ave, Tampa, FL 33613, USA
J Neuroimmunol 132:164-72. 2002.... - Increased vulnerability to focal ischemic brain injury in human apolipoprotein E4 knock-in miceTakashi Mori
Institute of Laboratory Animal Science, Department of Neurosurgery, Saitama Medical Center School, Kawagoe, Saitama, Japan
J Neuropathol Exp Neurol 62:280-91. 2003..Taken together, our results show that apoE affects the outcome of acute brain damage in an isoform-specific fashion (apoE4 > apoE3 = apoE2) in genetically engineered mice... - CD40-CD40L interaction in Alzheimer's diseaseJun Tan
The Roskamp Institute, Department of Psychiatry, University of South Florida, 3515 East Fletcher Avenue, Tampa, Florida 33613, USA
Curr Opin Pharmacol 2:445-51. 2002..Conversely, the finding that reduced CD40-CD40L interaction is associated with reduced chronic microgliosis and Tau hyperphosphorylation supports the view that, in general, mechanisms that reduce microgliosis will be beneficial in AD... - Role of CD40 ligand in amyloidosis in transgenic Alzheimer's miceJun Tan
The Roskamp Institute, Department of Psychiatry, University of South Florida, 3515 East Fletcher Avenue, Tampa, Florida 33613, USA
Nat Neurosci 5:1288-93. 2002..These findings suggest several possible mechanisms underlying mitigation of AD pathology in response to CD40L depletion, and validate the CD40-CD40L interaction as a target for therapeutic intervention in AD... - ADAM10 activation is required for green tea (-)-epigallocatechin-3-gallate-induced alpha-secretase cleavage of amyloid precursor proteinDemian F Obregon
Neuroimmunology Laboratory, Silver Child Development Center, Department of Psychiatry and Behavioral Medicine, The Byrd Alzheimer s Center and Research Institute, 3515 E Fletcher Avenue, Tampa, FL 33647, USA
J Biol Chem 281:16419-27. 2006..Thus, ADAM10 represents an important pharmacotherapeutic target for the treatment of cerebral amyloidosis in Alzheimer disease... - Arundic Acid ameliorates cerebral amyloidosis and gliosis in Alzheimer transgenic miceTakashi Mori
Institute of Medical Science, Saitama Medical School, 1981 Kamoda, Kawagoe, Saitama 350-8550, Japan
J Pharmacol Exp Ther 318:571-8. 2006..Based on the above results, arundic acid is considered to deserve further exploration as a promising therapeutic agent for AD... - Peripherally administered human umbilical cord blood cells reduce parenchymal and vascular beta-amyloid deposits in Alzheimer miceWilliam V Nikolic
Rashid Laboratory for Developmental Neurobiology, Silver Child Development Center, Department of Psychiatry and Behavioral Medicine, University of South Florida, Tampa, FL 33613, USA
Stem Cells Dev 17:423-39. 2008..Increased microglial phagocytic activity in this scenario was inhibited by addition of recombinant CD40L protein. These data suggest that HUCBC infusion mitigates AD-like pathology by disrupting CD40L activity... - Drak2 contributes to West Nile virus entry into the brain and lethal encephalitisShuhui Wang
Department of Microbiology, Immunology and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, USA
J Immunol 181:2084-91. 2008..These results suggest that following a systemic infection, WNV might cross the blood brain barrier and enter the CNS by being carried by infected infiltrating T cells... - Transcutaneous beta-amyloid immunization reduces cerebral beta-amyloid deposits without T cell infiltration and microhemorrhageWilliam V Nikolic
Department of Psychiatry and Behavioral Medicine, University of South Florida, Tampa, FL 33613, USA
Proc Natl Acad Sci U S A 104:2507-12. 2007..Together, these data suggest that t.c. immunization constitutes an effective and potentially safe treatment strategy for AD... - Overexpression of human S100B exacerbates brain damage and periinfarct gliosis after permanent focal ischemiaTakashi Mori
Institute of Medical Science, Saitama Medical Center University, 1981 Kamoda, Kawagoe, Saitama 350 8550, Japan
Stroke 39:2114-21. 2008..Furthermore, we have suggested that the astrocyte-derived protein S100B may be important in these pathogenic events. However, the causal relationship between S100B and exacerbation of brain damage in vivo remains to be elucidated... - NSAIDs for the chemoprevention of Alzheimer's diseaseChristine A Szekely
Department of Mental Health, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA
Subcell Biochem 42:229-48. 2007..The feasibility of using NSAIDs as a chemopreventive agent in AD is discussed... - Control of toll-like receptor 7 expression is essential to restrict autoimmunity and dendritic cell proliferationJonathan A Deane
Laboratory of Immunogenetics, NIAID NIH, Rockville, MD 20852, USA
Immunity 27:801-10. 2007..These results underscore the importance of tightly regulating expression of TLR7 to prevent spontaneous triggering of harmful autoreactive and inflammatory responses...