Virginia M SandersSummaryAffiliation: Loyola University Medical Center Country: USA Publications
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Norepinephrine, the beta-adrenergic receptor, and immunityVirginia M Sanders
Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Medical Center, Stritch School of Medicine, Maywood, Illinois 60153, USA
Brain Behav Immun 16:290-332. 2002....- CD4+ T, but not CD8+ or B, lymphocytes mediate facial motoneuron survival after facial nerve transectionCraig J Serpe
Department of Cell Biology, Neurobiology and Anatomy, Loyola University Medical Center, 2160 South First Avenue, Maywood, Illinois 60153, USA
Brain Behav Immun 17:393-402. 2003..5 and 63%+/-1.0, respectively). It is concluded that, of the population of FMN that do not survive injury, CD4+ T lymphocytes, but not CD8+ T lymphocytes or B cells, mediate FMN survival after peripheral nerve injury... - Role of the immune system in the maintenance of mouse facial motoneuron viability after nerve injuryKathryn J Jones
Department of Cell Biology, Neurobiology and Anatomy, Loyola University Chicago, Maywood, IL 60153, USA
Brain Behav Immun 19:12-9. 2005.... 
CD4-positive T cell-mediated neuroprotection requires dual compartment antigen presentationSusanna C Byram
Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Chicago, Maywood, Illinois 60153, USA
J Neurosci 24:4333-9. 2004..This is the first in vivo report demonstrating a neuroprotective mechanism requiring APC functions by resident (i.e., parenchymal) microglial cells...- Immune-mediated neuroprotection of axotomized mouse facial motoneurons is dependent on the IL-4/STAT6 signaling pathway in CD4(+) T cellsCynthia A Deboy
Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Chicago, 2160 S 1st Avenue, Maywood, IL 60153, USA
Exp Neurol 201:212-24. 2006..Collectively, these data suggest that STAT6-mediated CD4(+) T cell differentiation into the Th2 subset is necessary for FMN survival. A hypothesis relevant to motoneuron disease progression is presented... - Phenotype of CD4+ T cell subsets that develop following mouse facial nerve axotomyJunping Xin
Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Medical Center, Maywood, IL 60153, USA
Brain Behav Immun 22:528-37. 2008.... - CD4+CD25+ regulatory T cells and CD1-restricted NKT cells do not mediate facial motoneuron survival after axotomyCynthia A Deboy
Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Chicago, Maywood, IL 60153, and Research and Development Service, Hines VA Hospital 60141, USA
J Neuroimmunol 176:34-8. 2006.... - Effects of facial nerve axotomy on Th2- and Th1-associated chemokine expression in the facial motor nucleus of wild-type and presymptomatic mSOD1 miceDerek A Wainwright
Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Medical Center, Maywood, IL 60153, USA
J Neuroimmunol 216:66-75. 2009..Differences in the number of CCL11- and CXCL11-expressing cells were observed between WT and mSOD1 mice after facial nerve axotomy... - Functional recovery and facial motoneuron survival are influenced by immunodeficiency in crush-axotomized miceTaylor Beahrs
Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Medical Center, Maywood, IL 60153, USA
Exp Neurol 221:225-30. 2010.... - Toll-like receptor 2 and facial motoneuron survival after facial nerve axotomyDerek A Wainwright
Dept of Cell Biology, Neurobiology, and Anatomy, Loyola University Medical Center, Maywood, IL 60153, United States
Neurosci Lett 471:10-4. 2010..These data contribute to understanding the role of innate immunity after FMN death and may be relevant to motoneuron diseases, such as amyotrophic lateral sclerosis (ALS)... - Functional recovery after facial nerve crush is delayed in severe combined immunodeficient miceCraig J Serpe
Department of Cell Biology, Neurobiology and Anatomy, Loyola University Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
Brain Behav Immun 16:808-12. 2002..5+/-0.3 and 10.0+/-0.0 days, respectively. These results suggest that the delayed behavioral recovery time observed in scid mice may be due to the absence of T and B lymphocytes... - Natural killer cells do not mediate facial motoneuron survival after facial nerve transectionSusanna C Byram
Department of Cell Biology, Neurobiology and Anatomy, Loyola University Medical Center, 2160 South First Avenue, Maywood, IL 60153, USA
Brain Behav Immun 17:417-25. 2003..Thus, NK cells appear to not be a component of immune cell-mediated rescue of motoneurons from axotomy induced cell death... - Use of laser microdissection in the investigation of facial motoneuron and neuropil molecular phenotypes after peripheral axotomyNichole A Mesnard
Neuroscience Program, Loyola University Medical Center, Maywood, IL 60153, USA
Exp Neurol 225:94-103. 2010.... - B cell receptor- and beta 2-adrenergic receptor-induced regulation of B7-2 (CD86) expression in B cellsAdam P Kohm
Department of Cell Biology, Loyola University Stritch School of Medicine, Maywood, IL 60153, USA
J Immunol 168:6314-22. 2002..Thus, this study provides additional insight into the signaling intermediates and molecular mechanisms by which stimulation of the BCR and beta(2)AR may regulate B cell-associated B7-2 expression... - Adaptive immunity in mice lacking the beta(2)-adrenergic receptorVirginia M Sanders
Department of Cell Biology, Neurobiology and Anatomy, Loyola University Medical Center, Maywood, IL 60153, USA
Brain Behav Immun 17:55-67. 2003.... - It takes nerve to tell T and B cells what to doNicholas W Kin
Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, OH 43210, USA
J Leukoc Biol 79:1093-104. 2006..We will also discuss how dysregulation of this line of communication between the nervous and immune systems might contribute to disease development and progression... - Role of immunity in recovery from a peripheral nerve injuryVirginia M Sanders
Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University School of Medicine and Public Health, 2194 Graves Hall, 333 W 10th Avenue, Columbus, OH 43210, USA
J Neuroimmune Pharmacol 1:11-9. 2006.... - Brain-derived neurotrophic factor supports facial motoneuron survival after facial nerve transection in immunodeficient miceCraig J Serpe
Rehabilitation, Research and Development Service, Hines VA Hospital, 5th and Roosevelt Road, Hines, IL 60141, USA
Brain Behav Immun 19:173-80. 2005..3) 4 wpo. These data lend support to the hypothesis that CD4+ T cells produce NTF that support motoneuron survival before target reconnection occurs... - CD86 regulates IgG1 production via a CD19-dependent mechanismNicholas W Kin
Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, OH 43210
J Immunol 179:1516-23. 2007..Thus, our findings suggest that CD86 plays a key role in regulating the level of IgG(1) produced in vitro and in vivo, and that Lyn and CD19 may be the signaling intermediates activated by CD86 proximal to PI3K... - Impaired antibody synthesis after spinal cord injury is level dependent and is due to sympathetic nervous system dysregulationKurt M Lucin
The Integrated Biomedical Science Graduate Program, The Ohio State University College of Medicine, Columbus, OH 43210, USA
Exp Neurol 207:75-84. 2007..These data illustrate the immunosuppressive effects of the SNS after high-level SCI and indicate that immune deficits may be overcome using beta-blockers... - Spinal cord injury triggers systemic autoimmunity: evidence for chronic B lymphocyte activation and lupus-like autoantibody synthesisDaniel P Ankeny
Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University College of Medicine, Columbus, Ohio 43210, USA
J Neurochem 99:1073-87. 2006..We show a similar pathologic potential for the autoantibodies produced after SCI. Thus, mammalian SCI produces marked dysregulation of B cell function (i.e. autoimmunity) with pathological potential... - CXCR3-/- mice mount an efficient Th1 response but fail to control Leishmania major infectionLucia E Rosas
Department of Microbiology, The Ohio State University, Columbus, Ohio 43221, USA
Eur J Immunol 35:515-23. 2005..major is due to impaired CD4+ and CD8+ T cell trafficking and decreased production of IFN-gamma at the site of infection rather than to their inability to mount a parasite-specific Th1 response... - Interdisciplinary research: noradrenergic regulation of adaptive immunityVirginia M Sanders
Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University Medical Center, Columbus, OH, USA
Brain Behav Immun 20:1-8. 2006..And finally, this review will discuss how the lessons from the past can help us to attain a vision of interdisciplinary research for the future... - Autonomic innervation and regulation of the immune system (1987-2007)Dwight M Nance
Susan Samueli Center for Integrative Medicine, University of California Irvine, Orange, CA 92868 4283, USA
Brain Behav Immun 21:736-45. 2007.... - The level of IgE produced by a B cell is regulated by norepinephrine in a p38 MAPK- and CD23-dependent mannerGeorg Pongratz
Department of Molecular Virology, Immunology, and Medical Genetics, Ohio State University, Columbus, OH 43210, USA
J Immunol 177:2926-38. 2006.... - CD86 and beta2-adrenergic receptor stimulation regulate B-cell activity cooperativelyJoseph R Podojil
Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, OH 43210, USA
Trends Immunol 26:180-5. 2005..This finding suggests that signaling pathways that are activated by an immunoreceptor (CD86) and a neuroreceptor (beta2AR) converge to regulate the IgG1 response... - CD86 stimulation on a B cell activates the phosphatidylinositol 3-kinase/Akt and phospholipase C gamma 2/protein kinase C alpha beta signaling pathwaysNicholas W Kin
Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, OH 43210, USA
J Immunol 176:6727-35. 2006..These results identify a previously unknown signaling pathway induced by CD86 to regulate the level of B cell gene expression and activity... - CD86 and beta2-adrenergic receptor signaling pathways, respectively, increase Oct-2 and OCA-B Expression and binding to the 3'-IgH enhancer in B cellsJoseph R Podojil
Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, Ohio 43210, USA
J Biol Chem 279:23394-404. 2004.... - Selective regulation of mature IgG1 transcription by CD86 and beta 2-adrenergic receptor stimulationJoseph R Podojil
Department of Molecular Virology, Immunology, and Medical Genetics, Ohio State University, Columbus, OH 43210, USA
J Immunol 170:5143-51. 2003..These results provide the first evidence that CD86 and/or beta(2)AR stimulation on a CD40 ligand/IL-4-activated B cell increases the level of IgG1 protein produced per cell by increasing the rate of mature IgG1 transcription... - Epigenetic regulation of Th1 and Th2 cell developmentVirginia M Sanders
Department of Molecular Virology, Immunology and Medical Genetics, The Ohio State University Medical Center, Columbus, OH, USA
Brain Behav Immun 20:317-24. 2006..This article will review basic epigenetic mechanisms and what is known about how these mechanisms influence cytokine gene expression in a naïve CD4+ T cell as it develops into a Th1 or Th2 cell...