| First Author | Telieps T | Year | 2013 |
| Journal | Eur J Immunol | Volume | 43 |
| Issue | 6 | Pages | 1499-510 |
| PubMed ID | 23505065 | Mgi Jnum | J:198120 |
| Mgi Id | MGI:5495564 | Doi | 10.1002/eji.201242819 |
| Citation | Telieps T, et al. (2013) Cellular-FLIP, Raji isoform (c-FLIPR ) modulates cell death induction upon T-cell activation and infection. Eur J Immunol 43(6):1499-510 |
| abstractText | Dysregulation of apoptosis caused by an imbalance of pro- and anti-apoptotic protein expression can lead to cancer, neurodegenerative, and autoimmune diseases. Cellular-FLIP (c-FLIP) proteins inhibit apoptosis directly at the death-inducing signaling complex of death receptors, such as CD95, and have been linked to apoptosis regulation during immune responses. While the isoforms c-FLIPL and c-FLIPS are well characterized, the function of c-FLIPR remains poorly understood. Here, we demonstrate the induction of endogenous murine c-FLIPR in activated lymphocytes for the first time. To analyze c-FLIPR function in vivo, we generated transgenic mice expressing murine c-FLIPR specifically in hematopoietic cells. As expected, lymphocytes from c-FLIPR transgenic mice were protected against CD95-induced apoptosis in vitro. In the steady state, transgenic mice had normal cell numbers and unaltered frequencies of B cells and T-cell subsets in lymphoid organs. However, when challenged with Listeria monocytogenes, c-FLIPR transgenic mice showed less liver necrosis and better bacterial clearance compared with infected wild-type mice. We conclude that c-FLIPR expression in hematopoietic cells supports an efficient immune response against bacterial infections. |
