Research Topics
Genomes and Genes
| Jaime ImitolaSummaryAffiliation: Harvard University Country: USA Publications
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Detail Information
Publications
Prospects for neural stem cell-based therapies for neurological diseasesJaime Imitola
Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Neurotherapeutics 4:701-14. 2007....
Localizing central nervous system immune surveillance: meningeal antigen-presenting cells activate T cells during experimental autoimmune encephalomyelitisPia Kivisakk
Center for Neurological Diseases, Brigham and Women s Hospital, Department of Neurology, Harvard Medical School, Boston, MA 02115, USA
Ann Neurol 65:457-69. 2009..We hypothesized that activated CD4(+) T cells gain direct access to the subarachnoid space and become reactivated on encounter with cognate antigen in this compartment...- Reversible neural stem cell niche dysfunction in a model of multiple sclerosisStine Rasmussen
Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Ann Neurol 69:878-91. 2011..We hypothesized that chronic microglia activation contributes to the failure of the NSC repair potential in the SVZ... - Elevated neuronal expression of CD200 protects Wlds mice from inflammation-mediated neurodegenerationTanuja Chitnis
Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, MA 02115, USA
Am J Pathol 170:1695-712. 2007..Strategies that up-regulate the expression of CD200 in the CNS or molecules that ligate the CD200R may be relevant as neuroprotective strategies in multiple sclerosis... - Differential role of programmed death-ligand 1 [corrected] and programmed death-ligand 2 [corrected] in regulating the susceptibility and chronic progression of experimental autoimmune encephalomyelitisBing Zhu
Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
J Immunol 176:3480-9. 2006..In conclusion, PD-L1 and PD-L2 differentially regulate the susceptibility and chronic progression of EAE in a strain-specific manner... - Transcriptional therapy with the histone deacetylase inhibitor trichostatin A ameliorates experimental autoimmune encephalomyelitisSandra Camelo
Laboratory of Transcriptional and Immune Regulation, Brigham and Women's Hospital, Department of Neurology, Harvard Medical School, Boston, MA 02139, USA
J Neuroimmunol 164:10-21. 2005..A transcriptional imbalance in MS may contribute to immune dysregulation and neurodegeneration, and we identify HDAC inhibition as a transcriptional intervention to ameliorate this imbalance... - Paradoxical dysregulation of the neural stem cell pathway sonic hedgehog-Gli1 in autoimmune encephalomyelitis and multiple sclerosisYue Wang
Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
Ann Neurol 64:417-27. 2008..Here, we asked how central nervous system inflammatory injury regulates the intrinsic properties of NSCs and their niches... - Distinct functions of autoreactive memory and effector CD4+ T cells in experimental autoimmune encephalomyelitisWassim Elyaman
Center for Neurologic Diseases, Brigham and Women s Hospital, Boston, MA 02115, USA
Am J Pathol 173:411-22. 2008..Our data extend the understanding of the pathogenicity of autoreactive memory T cells and have important implications for the development of novel therapies for human autoimmune diseases... - Persistent activation of microglia is associated with neuronal dysfunction of callosal projecting pathways and multiple sclerosis-like lesions in relapsing--remitting experimental autoimmune encephalomyelitisStine Rasmussen
Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Brain 130:2816-29. 2007..These features closely mimic the periventricular and cortical pathology described in MS patients and establish a model that could be useful to study mechanisms of progression in MS... - Directed migration of neural stem cells to sites of CNS injury by the stromal cell-derived factor 1alpha/CXC chemokine receptor 4 pathwayJaime Imitola
Center for Neurologic Diseases, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 101:18117-22. 2004..CXCR4 expression within germinal zones suggests that NSC homing after injury and migration during development may invoke similar mechanisms... - Galectin-1 deactivates classically activated microglia and protects from inflammation-induced neurodegenerationSarah C Starossom
Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Immunity 37:249-63. 2012..Thus, Gal1-glycan interactions are essential in tempering microglial activation, brain inflammation, and neurodegeneration, with critical therapeutic implications for MS... - Differential engagement of Tim-1 during activation can positively or negatively costimulate T cell expansion and effector functionSheng Xiao
Center for Neurologic Diseases, Brigham and Women s Hospital and Children s Hospital Boston, Harvard Medical School, Boston, MA 02115, USA
J Exp Med 204:1691-702. 2007..These data indicate that Tim-1 regulates T cell responses and that Tim-1 engagement can alter T cell function depending on the affinity/avidity with which it is engaged... - Subventricular zone microglia transcriptional networksSarah C Starossom
Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Brain Behav Immun 25:991-9. 2011..Our data demonstrate for the first time, distinct transcriptional networks of microglia activation in vivo, that suggests a role as mediators of injury or repair... - The Tim-3 ligand galectin-9 negatively regulates T helper type 1 immunityChen Zhu
Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Nat Immunol 6:1245-52. 2005..These data suggest that the Tim-3-galectin-9 pathway may have evolved to ensure effective termination of effector T(H)1 cells... - Neural stem cells rescue nervous purkinje neurons by restoring molecular homeostasis of tissue plasminogen activator and downstream targetsJianxue Li
Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
J Neurosci 26:7839-48. 2006..This report demonstrates for the first time that NSCs can rescue imperiled host neurons by rectifying their gene expression, elevating somatic stem cell therapeutic potential beyond solely cell replacement strategy... - IL-9 induces differentiation of TH17 cells and enhances function of FoxP3+ natural regulatory T cellsWassim Elyaman
Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, Boston, MA 02115, USA
Proc Natl Acad Sci U S A 106:12885-90. 2009..The mechanism of IL-9 effects on T(H)17 and T(regs) is through activation of STAT3 and STAT5 signaling. Our findings highlight a role of IL-9 as a regulator of pathogenic versus protective mechanisms of immune responses... - Multimodal coherent anti-Stokes Raman scattering microscopy reveals microglia-associated myelin and axonal dysfunction in multiple sclerosis-like lesions in miceJaime Imitola
Brigham and Women s Hospital, Center for Neurologic Diseases, Partner Multiple Sclerosis Center, Harvard Medical School, Department of Neurology, Boston, Massachusetts 02115, USA
J Biomed Opt 16:021109. 2011.... - Human glioma growth is controlled by microRNA-10bGalina Gabriely
Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
Cancer Res 71:3563-72. 2011..Altogether, our experiments validate an important role of miR-10b in gliomagenesis, reveal a novel mechanism of miR-10b-mediated regulation, and suggest the possibility of its future use as a therapeutic target in gliomas... - Th1 cytokines, programmed cell death, and alloreactive T cell clone size in transplant toleranceKoji Kishimoto
Laboratory of Immunogenetics and Transplantation, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA
J Clin Invest 109:1471-9. 2002..These data have implications for the design of tolerance strategies in transplant recipients with varying degrees of MHC mismatching... - Insights into the molecular pathogenesis of progression in multiple sclerosis: potential implications for future therapiesJaime Imitola
Center for Neurologic Diseases and Partners Multiple Sclerosis Center, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA
Arch Neurol 63:25-33. 2006..The molecular pathways leading to structural and functional neurodegeneration and those that prevent regeneration need to be identified in order to design new therapeutic strategies that can halt or even reverse disease progression... - Corticotropin-releasing hormone contributes to the peripheral inflammatory response in experimental autoimmune encephalomyelitisChristina Benou
Center for Neurologic Diseases, Brigham and Women s Hospital and Harvard Medical School, Boston, MA 02115, USA
J Immunol 174:5407-13. 2005..We conclude that peripheral CRH exerts a proinflammatory effect in EAE with a selective increase in Th1-type responses. These findings have implications for the treatment of Th1-mediated diseases such as multiple sclerosis... - The cell cycle associated protein, HTm4, is expressed in differentiating cells of the hematopoietic and central nervous system in miceJeffery L Kutok
Department of Pathology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, 02115, USA
J Mol Histol 36:77-87. 2005..In addition, we observed that murine HTm4 is highly expressed in the developing and adult murine nervous system, suggesting a previously unrecognized role in central and peripheral nervous system development... - Expression of Cux-1 and Cux-2 in the subventricular zone and upper layers II-IV of the cerebral cortexMarta Nieto
Department of Neurology, Harvard Medical School and Howard Hughes Medical Institute, Beth Israel Deaconess Medical Center, Boston, Massachusetts 02115, USA
J Comp Neurol 479:168-80. 2004..The patterns of expression of Cux genes suggest potential roles as determinants of the neuronal fate of the upper cortical layer neurons... 
Neural stem cells and the future treatment of neurological diseases: raising the standardJaime Imitola
Center for Neurologic Diseases, Department of Neurology, Brigham and Women s Hospital, Harvard Medical School, Boston, MA, USA
Methods Mol Biol 438:9-16. 2008..Addressing these challenges is crucial for translation of neural stem cell therapy to the clinic...- Microglia-mediated nitric oxide cytotoxicity of T cells following amyloid beta-peptide presentation to Th1 cellsAlon Monsonego
Center for Neurologic Diseases, Brigham and Women s Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, HIM 730, Boston, MA 02115, USA
J Immunol 171:2216-24. 2003..Furthermore, Th2 type T cell responses may have a beneficial effect on this process by down-regulation of NO and the proinflammatory environment... - Stem cells: cross-talk and developmental programsJaime Imitola
Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Boston, MA4 02115, USA
Philos Trans R Soc Lond B Biol Sci 359:823-37. 2004..Understanding the relevant molecular pathways of stem cell repair phenotype should be a priority, in our view, for the entire stem cell field... - Critical role of the programmed death-1 (PD-1) pathway in regulation of experimental autoimmune encephalomyelitisAlan D Salama
Laboratory of Immunogenetics and Transplantation, Children's Hospital, Harvard Medical School, Boston, MA 02115, USA
J Exp Med 198:71-8. 2003..Interestingly, PD-L2 but not PD-L1 blockade in WT animals also resulted in disease augmentation. Our data are the first demonstration that the PD-1 pathway plays a critical role in regulating EAE... - Cytokines in multiple sclerosis: from bench to bedsideJaime Imitola
Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, 77 Avenue Louis Pasteur, Rm 710, Boston, MA 02115, USA
Pharmacol Ther 106:163-77. 2005..In this review, we will summarize the current knowledge on the role of cytokine pathways in MS and what we learned from investigation of its animal model: experimental autoimmune encephalomyelitis (EAE)... - Neural stem/progenitor cells express costimulatory molecules that are differentially regulated by inflammatory and apoptotic stimuliJaime Imitola
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, USA
Am J Pathol 164:1615-25. 2004.... - Mechanisms of Disease: the role of stem cells in the biology and treatment of gliomasJörg Dietrich
Department of Neurology, Brigham and Women s Hospital, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02115, USA
Nat Clin Pract Oncol 5:393-404. 2008..This Review summarizes recent advances in the basic understanding of neural stem cell and cancer stem cell biology and the progress towards translating these novel concepts into the clinic... - Mutations in ARFGEF2 implicate vesicle trafficking in neural progenitor proliferation and migration in the human cerebral cortexVolney L Sheen
Division of Neurogenetics and Howard Hughes Medical Institute, Department of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02115, USA
Nat Genet 36:69-76. 2004..Our findings show that vesicle trafficking is an important regulator of proliferation and migration during human cerebral cortical development... - Genetic programs and responses of neural stem/progenitor cells during demyelination: potential insights into repair mechanisms in multiple sclerosisJaime Imitola
Center for Neurologic Diseases, Partners MS Center, Department of Neurology, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA
Physiol Genomics 14:171-97. 2003..Emerging knowledge of the molecules that may be involved in such responses may help in the design of future stem cell-based treatment of demyelinating diseases such as multiple sclerosis... - Abeta-induced meningoencephalitis is IFN-gamma-dependent and is associated with T cell-dependent clearance of Abeta in a mouse model of Alzheimer's diseaseAlon Monsonego
National Institute of Biotechnology and Department of Microbiology and Immunology, Faculty of Health Sciences, Ben Gurion University, Beer Sheva 84105, Israel
Proc Natl Acad Sci U S A 103:5048-53. 2006.... - Neural stem cell biology may be well suited for improving brain tumor therapiesStephen Yip
The Burnham Institute, Program in Developmental and Regenerative Cell Biology, La Jolla, California 92037, USA
Cancer J 9:189-204. 2003..It is important to emphasize, however, that the use of NSCs is adjunctive and is not a replacement for other therapies that should be used in parallel... - Genomic and functional profiling of human Down syndrome neural progenitors implicates S100B and aquaporin 4 in cell injuryGiuseppe Esposito
Department of Human Physiology and Pharmacology, Vittorio Erspamer Faculty of Pharmacy, University of Rome La Sapienza, Rome, Italy
Hum Mol Genet 17:440-57. 2008....