| First Author | Huber S | Year | 2006 |
| Journal | Immunology | Volume | 119 |
| Issue | 4 | Pages | 541-50 |
| PubMed ID | 17010108 | Mgi Jnum | J:118533 |
| Mgi Id | MGI:3699746 | Doi | 10.1111/j.1365-2567.2006.02469.x |
| Citation | Huber S, et al. (2006) Reduced myocarditis following Coxsackievirus infection in cellular FLICE inhibitory protein--long form-transgenic mice. Immunology 119(4):541-50 |
| abstractText | Cellular FLICE inhibitory protein--long form (c-FLIP(L)) is a caspase-defective homologue of caspase-8 that blocks apoptosis by death receptors. c-FLIP(L) expression in T cells can also augment activation of the mitogen-activated protein kinase, extracellular signal-related kinase, as well as nuclear factor-kappaB. This contributes to increased production of interleukin-2 and CD25, resulting in hyperproliferation of T cells from c-FLIP(L)-transgenic mice. c-FLIP also heterodimerizes with and activates caspase-8, resulting in increased death of T cells and a selection of a T helper 2 cytokine profile. The effects of c-FLIP on cytolytic function of CD8(+) T cells have not been examined previously. We studied the cytolytic capacity of T cells from c-FLIP(L)-transgenic mice using an antigen-specific system, as well as the consequences during a viral immune response to Coxsackievirus B3 (CVB3). The increased T-cell receptor (TCR) signalling due to c-FLIP did not alter the cytolytic machinery but did reduce cytotoxicity because of decreased surface expression of TCR and CD8. It also produced a Tc2 cytokine profile. These effects of c-FLIP collectively served to diminish the severity of CVB3-induced myocarditis. |
