Why the study?
Do TCR Vbeta-derived peptides improve resistance to cardiac pathology in aged mice infected with coxsackievirus?
Do TCR Vbeta-derived peptides improve resistance to cardiac pathology in aged mice infected with coxsackievirus?
TCR Vbeta-derived peptides may offer a novel immunomodulatory approach to reverse immunosenescence and protect against viral-induced cardiac pathology in preclinical models.
May guide immunomodulation in aged viral myocarditis; leaves open human translation from murine data.
The operation of the immune system is a complex orchestration of specific self and non-self-recognition capacities mediated by cells of the innate system acting in coordination with T and B lymphocytes in a series of processes modulated by cytokines. We provide evidence for a natural immunomodulatory system involving autoantibodies directed against a controlling segment of T cell receptor Vbeta chains that downregulate production of stimulatory cytokines balanced by the peptides which in turn upregulate inflammatory activities mediated by TH1-type helper cells. TCR Vbeta-derived peptides effective in retrovirally induced immunosupression could also reverse the effects of immunosenescence in aged mice by restoring the balance of TH1- and TH2-type immunity and the resistance of the animals to cardiac pathology caused by infection with coxsackievirus. An unexpected finding was an adaptive role of the T cells from peptide-treated mice in remodeling damaged hearts by increasing net collagen synthesis by cardiac fibroblasts.
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Marchalonis et al. (2005) studied this question.
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