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

Persistent Link:
http://hdl.handle.net/10150/194700
Title:
T-cell Receptor Vβ8.1 Peptide Reduces Coxsackievirus-induced Cardiopathology During Murine Acquired Immunodeficiency Syndrome and Aging.
Author:
Sepulveda, Ramon Tomas
Issue Date:
2005
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
Keywords:
HIV; AIDS; MAIDS; LP-BM5; Coxsackievirus; Immunotherapy
Degree Name:
PhD
Degree Level:
doctoral
Degree Program:
Microbiology & Immunology; Graduate College
Degree Grantor:
University of Arizona
Committee Chair:
Marchalonis, John J.

Full metadata record

DC FieldValue Language
dc.language.isoENen_US
dc.titleT-cell Receptor Vβ8.1 Peptide Reduces Coxsackievirus-induced Cardiopathology During Murine Acquired Immunodeficiency Syndrome and Aging.en_US
dc.creatorSepulveda, Ramon Tomasen_US
dc.contributor.authorSepulveda, Ramon Tomasen_US
dc.date.issued2005en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © 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.en_US
dc.description.abstractInfection 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.en_US
dc.typetexten_US
dc.typeElectronic Dissertationen_US
dc.subjectHIVen_US
dc.subjectAIDSen_US
dc.subjectMAIDSen_US
dc.subjectLP-BM5en_US
dc.subjectCoxsackievirusen_US
dc.subjectImmunotherapyen_US
thesis.degree.namePhDen_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineMicrobiology & Immunologyen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.chairMarchalonis, John J.en_US
dc.contributor.committeememberPayne, Claireen_US
dc.contributor.committeememberAhmad, Nafeesen_US
dc.contributor.committeememberBernstein, Harrisen_US
dc.contributor.committeememberWatson, Ronald R.en_US
dc.identifier.proquest1364en_US
dc.identifier.oclc137355259en_US
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