T-cell receptor V beta 8.1 peptide reduces coxsackievirus-induced cardiopathology during murine acquired immunodeficiency syndrome.
Infection of people with human immunodeficiency virus (HIV) as well as LP-BM5 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 (T(H)1) and T-helper 2 (T(H) 2) response subsets. In murine acquired immunodeficiency syndrome (AIDS), T(H)1 deficiency enables the host to be susceptible to coxsackievirus infection, inducing cardiopathology in a short period. T-cell receptor (TCR) Vbeta8.1 peptide, a 16-mer peptide containing the entire CDR1 segment and part of the FR2 region of human Vbeta8, showed both an immunoregulating and immunostimulating effect in murine AIDS. TCR Vbeta8.1 peptide acts on T cells promoting interleukin-2 production and therefore enhancing a cell-mediated 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.
Sepúlveda
Ramón Tomás
RT
College of Public Health, College of Medicine, University of Arizona, Tucson, Arizona 85724, USA.
Marchalonis
John Jacob
JJ
Watson
Ronald Ross
RR
D000595:Amino Acid Sequence; D000818:Animals; D003384:Coxsackievirus Infections / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D029822:Enterovirus B, Human / Q000276:immunology*; D005260:Female; D051379:Mice; D008810:Mice, Inbred C57BL; D008969:Molecular Sequence Data; D016183:Murine Acquired Immunodeficiency Syndrome / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D009206:Myocardium / Q000276:immunology / Q000473:pathology*; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000627:therapeutic use*
D016693:Receptors, Antigen, T-Cell, alpha-beta; C113249:T cell receptor peptide Vbeta8.1