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    T-cell Receptor Vβ8.1 Peptide Reduces Coxsackievirus-induced Cardiopathology During Murine Acquired Immunodeficiency Syndrome and Aging.

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    Author
    Sepulveda, Ramon Tomas
    Issue Date
    2005
    Keywords
    HIV
    AIDS
    MAIDS
    LP-BM5
    Coxsackievirus
    Immunotherapy
    Committee Chair
    Marchalonis, John J.
    
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    Publisher
    The University of Arizona.
    Rights
    Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
    Abstract
    Infection of people with human immunodeficiency virus (HIV) as well as LPBM5 infection in mice results in progressive deterioration of the immune system in the majority of untreated hosts. Peptide immunotherapy has been shown to be effective in the stimulation or immunoregulation of T-helper 1 (TH1) and T-helper 2 (TH2) response subsets. In murine acquired immunodeficiency syndrome (AIDS), TH1 deficiency enables the host to be susceptible to coxsackievirus infection, inducing cardiopathology in a short period. T-cell receptor (TCR) Vβ8.1 peptide, a 16-mer peptide containing the entire CFR1 segment and part of the FR2 region of human Vβ8, showed both an immunoregulating and immunostimulating effect in murine AIDS. TCR Vβ8.1 peptide acts on T cells promoting interleukin-2 production and therefore enhancing a cellmediated immune response. It retarded development of cardiopathology due to coxsackievirus infection. Retrovirus infected mice treated with the peptide showed a longer life span than the nontreated retrovirus infected animals.
    Type
    text
    Electronic Dissertation
    Degree Name
    PhD
    Degree Level
    doctoral
    Degree Program
    Microbiology and Immunology
    Graduate College
    Degree Grantor
    University of Arizona
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