Coxsackievirus-induced disease. CD4+ cells initiate both myocarditis and pancreatitis in DBA/2 mice.

摘要: DBA/2 male mice inoculated intraperitoneally with 1.8 X 10(5) plaque-forming units (PFU) coxsackievirus B-3 (CVB3) showed extensive inflammatory cell infiltration of the myocardium and acinar tissue pancreas in 7 days. Selective depletion T lymphocyte subpopulations indicated that CD4 cells were either completely or partially responsible for damage both organs. Other organs such as liver infected contained virus titers equivalent to those seen heart but no apparent injury. The role was confirmed by positive selection subpopulation from CVB3-immune lymphocytes vitro adoptive transfer these into cell-deficient (thymectomized, irradiated, bone marrow reconstituted, TXBM) recipients. Lymphocytes CVB3-infected donor adsorbed myocyte, skin fibroblast, vascular endothelial (VEC) monolayers. adherent population retrieved adoptively transferred uninfected syngeneic When killed days later, animals receiving unfractionated immune eluted monolayers developed myocarditis pancreatitis. Anti-Thy 1.2 C' treatment abrogated disease. Cells fibroblast VEC pathogenicity. Adsorption presence anti-IAd (class II major histocompatibility complex antigen, MHC) inhibited attachment pathogenic cell, whereas anti KdDd (a class I MHC antigen) had effect.