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- W2086682857 abstract "Toll-like receptors (TLR) are pattern recognition receptors that are an essential feature of host defense against pathogens. Expression of TLR-4 on dendritic cells was reported to be required for initiation of experimental autoimmune myocarditis (EAM) but the mechanism by which TLR-4 signaling affects autoimmunity is incompletely understood. To determine the role of TLR-4 in EAM, wild type and TLR-4-/- mice were immunized with myosin peptide (614-629) in CFA. TLR-4-/- mice demonstrated decreased myosin specific proliferation and decreased production of INF-gamma and IL-2. Immunization with myosin induced greater severity of myocarditis in wild type compared to TLR-4-/- mice as evidenced by lesions in the myocardium. TcR Vbeta 8.1, 8.2+ CD4+ T cells, detected in lesions were isolated from splenocytes by flow cytometry and found to undergo increased apoptosis in TLR-4-/- mice. In situ immunohistochemistry showed increased colocalization of cleaved caspase 3 and TcR Vbeta 8.1, 8.2+ CD4+ T cells in TLR-4-/- mice compared to wild type. Increased apoptosis was associated with impaired activation of NF-kB p65 and decreased cell viability in the presence of TNF-alpha. These results demonstrate that infiltrating TcR Vbeta 8.1, 8.2+ CD4+ T cells are deleted by the mechanism of apoptosis in TLR-4-/- mice with EAM." @default.
- W2086682857 created "2016-06-24" @default.
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- W2086682857 date "2008-09-01" @default.
- W2086682857 modified "2023-09-27" @default.
- W2086682857 title "Inhibition of experimental autoimmune myocarditis: peripheral deletion of TcR Vβ 8.1, 8.2+ CD4+ T cells in TLR-4 deficient mice" @default.
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- W2086682857 doi "https://doi.org/10.1016/j.jaut.2008.06.002" @default.
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