Mae Lim
Stanford University
7 Papers
230 Citations
Mae Lim is an academic researcher from Stanford University. The author has contributed to research in topics: Antibody & Bordetella pertussis. The author has an hindex of 6, co-authored 7 publications.
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Papers
ADP-ribosyltransferase activity of pertussis toxin and immunomodulation by Bordetella pertussis
W. J. Black,J. J. Munoz,M. G. Peacock,PA Schad,JL Cowell,James J. Burchall,Mae Lim,Andrew D. Kent,Lawrence Steinman,Stanley Falkow +9 more
TL;DR: It is suggested that the ADP-ribosyltransferase activity is necessary for both pathogenicity and optimum immunoprotection in pertussis vaccine.
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Phase 1 clinical trial of chimeric monoclonal anti‐CD4 antibody in multiple sclerosis
J. W. Lindsey,Suzanne Hodgkinson,R. Mehta,R. C. Siegel,Dennis J. Mitchell,Mae Lim,Christopher Piercy,T. Tram,Leslie J. Dorfman,Dieter R. Enzmann,Lawrence Steinman +10 more
TL;DR: Treatment of MS patients with cM-T412 chimeric monoclonal anti-CD4 antibody is well tolerated at the doses tested and produces a long-lasting, selective depletion of CD4 lymphocytes.
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Pertussis toxin is required for pertussis vaccine encephalopathy
Lawrence Steinman,Alison A. Weiss,Nancy Adelman,Mae Lim,Richard Zuniga,John Oehlert,Erik L. Hewlett,Stanley Falkow +7 more
TL;DR: Purified pertussis toxin plus bovine serum albumin was tested and found to induce the lethal encephalopathy, demonstrating that the toxin was the critical constituent of B. pertussedis responsible for encephalitis.
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Prevention of experimental allergic encephalitis with in vivo administration of anti I-A antibody. Decreased accumulation of radiolabelled lymph node cells in the central nervous system.
TL;DR: Injection of anti I-A antibody in vivo prevented clinical EAE and decreased the accumulation of radiolabelled LNC in spinal cord after immunization with mouse spinal cord homogenate and adjuvants.
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Therapy of autoimmune diseases with antibody to immune response gene products or to T-cell surface markers.
Lawrence Steinman,Matthew K. Waldor,Scott S. Zamvil,Mae Lim,Leanore Herzenberg,Leonard A. Herzenberg,Hugh O. McDevitt,Dennis J. Mitchell,Subramaniam Sriram +8 more
TL;DR: In five models of autoimmune disease, monoclonal antibodies against products of the I-A subregion of the major histocompatibility complex or against the L3T4a molecule on helper/inducer T cells either prevented development of clinical signs or reversed ongoing disease when administered after clinical signs were apparent.
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