Fig 1.
IL-2-dependent expansion of Tregs during FV infection.
Depicted in brown are Treg activation events dependent on FV infection. No direct interactions between viral antigens and Tregs are required. Depicted in gray are required homeostatic signaling events for FV-induced Treg expansion. Homeostatic signaling levels are sufficient although FV infections may up-regulate expression of some membrane receptors. APC, antigen-presenting cell; FV, Friend virus; GITR, glucocorticoid-induced TNF receptor-related protein; GITRL, GITR ligand; IL-2, interleukin 2; TCR, T-cell receptor; TNFα, tumor necrosis factor α; Treg, regulatory T cell.
Fig 2.
IL-2-independent expansion of Tregs during FV infection.
Depicted in brown are Treg activation events dependent on FV infection. No direct interactions between exogenous viral antigens and Tregs are required. Depicted in gray are required homeostatic signaling events for FV-induced Treg expansion. FV infection indirectly up-regulates expression of TNFR2. FV, Friend virus; IL-2, interleukin 2; mb, membrane bound; Sag, superantigen; TNFR2, tumor necrosis factor receptor 2; Treg, regulatory T cell; Vβ5, T-cell receptor variable β chain 5.
Fig 3.
Duality of Treg effects in retroviral infections.
Deterimental effects are depicted in brown, and beneficial effects are depicted in gray. Arrows indicate effects, while blocked lines indicate blocked activities. FV, Friend virus; LP-BM5, murine retrovirus LP-BM5; SIV, simian immunodeficiency virus; Treg, regulatory T cell.