[BIC-announce] FW: Killam Lecture - TODAY - A Critical Role for Epitope Spreading in the EAE Model of Multiple Sclerosis: Implications for Human Immunotherapies
Jennifer Chew, Ms.
jennifer.chew at mcgill.ca
Tue Feb 12 12:29:48 EST 2008
PLEASE DISCARD IF THIS IS A DUPLICATE. THANK YOU. JENNIFER
________________________________
From: MNISTAFF - Montreal Neurological Institute Staff [mailto:MNISTAFF at LISTS.MCGILL.CA] On Behalf Of Enza Ferracane, Ms.
Sent: Tuesday, February 12, 2008 9:24 AM
To: MNISTAFF at LISTS.MCGILL.CA
Subject: Killam Lecture - TODAY
*****REMINDER*****
Killam Lecture:
Speaker:
Stephen D. Miller, Ph.D.
Judy Gugenheim Research Professor
Department of Microbiology-Immunology
Northwestern University Medical School
Title: "A Critical Role for Epitope Spreading in the EAE Model of Multiple Sclerosis: Implications for Human Immunotherapies".
Date: Tuesday, February 12, 2008
Place: de Grandpre Communications Centre
Time: 4:00 pm
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Dear colleagues,
Tomorrow's Killam seminar will be given by Dr. Stephen D. Miller from the Department of Microbiology-Immunology at Northwestern University Medical School.
Below is an overview of Dr. Miller's research and some of his papers.
Research Description
Cellular and molecular mechanisms of T cell tolerance; Pathogenesis and regulation of T cell-mediated autoimmune and virus-induced diseases; Mechanisms of virus-induced autoimmunity; Molecular mechanisms of costimulatory molecule interactions in T cell activation; Role of glial cells in antigen processing and presentation in the CNS.
Research Abstract
My laboratory investigates the cellular and molecular mechanisms of multiple aspects of the immunopathogenesis and specific immunoregulation of T cell-mediated autoimmune responses employing two mouse models of multiple sclerosis (MS) - Theiler's virus-induced demyelinating disease (a virus-induced model of MS) and Relapsing Experimental Autoimmune Encephalomyelitis (R-EAE) (an autoimmune model of MS).
Publications
Vanderlugt, C. L. and S. D. Miller. 2002.
Role of epitope spreading in immune-mediated diseases: Implications for immunotherapy.
Nature Rev. Immunol. 2:85-95.
Howard, L. M., S. Ostrovidov, C. E. Smith, M. C. Dal Canto, and S. D. Miller. 2002.
Normal Th1 development following long-term therapeutic blockade of CD154-CD40 in experimental autoimmune encephalomyelitis.
J. Clin. Invest. 109:233-241.
Rasley, A., K. L. Bost, J. K. Olson, S. D. Miller, and I. Marriott. 2002.
Expression of functional NK-1 receptors in murine microglia.
Glia 37:258-267.
Neville, K. L., J. Padilla, L. A. Matis, and S. D. Miller. 2002.
Myelin-specific tolerance attenuates the progression of a virus-induced demyelinating disease: Implications for the treatment of MS.
J. Neuroimmunol. 123:18-29.
Eagar, T. N., N. J. Karandikar, J. A. Bluestone, and S. D. Miller. 2002.
The role of CTLA-4 in induction and maintenance of peripheral T cell tolerance.
Eur. J. Immunol. 32:972-981.
Girvin, A. M., M. C. Dal Canto, and S. D. Miller. 2002.
CD40/CD40L interaction is essential for the induction of EAE in the absence of CD28-mediated costimulation.
J. Autoimmunity. 16:83-94.
Tompkins, S. M., J. Padilla, M. C. Dal Canto, J. P.-Y. Ting, L. Van Kaer, and S. D. Miller. 2002.
De novo CNS processing of myelin antigen is required for the initiation of EAE.
J. Immunol. 168:4173-4183.
Tompkins, S. M. and S. D. Miller. 2002.
An array of possibilities for multiple sclerosis.
Nature Med. 8:451-453.
Girvin, A. M., K. B. Gordon, C. J. Welsh, and S. D. Miller. 2002.
Differential abilities of central nervous system-resident endothelial cells and astrocytes to serve as inducible antigen presenting cells.
Blood. 99:3692-3701.
Tompkins, S. M., K. G. Fuller, and S. D. Miller. 2002.
Theilerís virus-mediated autoimmunity: Local presentation of CNS antigens and epitope spreading.
Ann. N.Y. Acad. Sci. 958:26-38.
Olson, J. K., T. N. Eagar, and S. D. Miller. 2002.
Functional activation of myelin-specific T cells by virus-induced molecular mimicry.
J. Immunol. 169:2719-2726.
Howard, L. M., M. C. Dal Canto, and S. D. Miller. 2002.
Transient anti-CD154-mediated immunotherapy of ongoing relapsing experimental autoimmune encephalomyelitis induces long-term inhibition of disease relapses.
J. Neuroimmunol. 129:58-65.
Kohm, A. P., P. A. Carpentier, H. A. Anger, and S. D. Miller. 2002.
Cutting Edge: CD4+CD25+ T regulatory cells suppress antigen-specific autoreactive immune responses and CNS inflammation during active experimental autoimmune encephalomyelitis.
J. Immunol. 169:4712-4716.
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