| First Author | Belhacéne N | Year | 2012 |
| Journal | PLoS One | Volume | 7 |
| Issue | 10 | Pages | e47321 |
| PubMed ID | 23071785 | Mgi Jnum | J:192226 |
| Mgi Id | MGI:5464190 | Doi | 10.1371/journal.pone.0047321 |
| Citation | Belhacene N, et al. (2012) Severe thymic atrophy in a mouse model of skin inflammation accounts for impaired TNFR1 signaling. PLoS One 7(10):e47321 |
| abstractText | Transgenic mice expressing the caspase-cleaved form of the tyrosine kinase Lyn (LynDeltaN) develop a TNFalpha-dependent skin disease that accurately recapitulates human psoriasis. Participation of lymphocytes in this disease was confirmed by backcrossing LynDeltaN mice on a Rag-1 deficient background. The present study was therefore conducted to analyze whether modification of lymphocyte homeostasis does occur and participate in the phenotype of LynDeltaN mice. We show here that LynDeltaN mice consistently exhibit thymic atrophy that correlates with both a net decrease in the CD4+/CD8+ Double Positive (DP) and an increase in Single Positive (SP) thymocyte sub-populations, but also display an increase of splenic mature B cell. Interestingly, a normal immune phenotype was rescued in a TNFR1 deficient background. Finally, none of these immune alterations was detected in newborn mice before the onset of inflammation. Therefore, we conclude that chronic inflammation can induce thymic atrophy and perturb spleen homeostasis in LynDeltaN mice through the increased production of TNFalpha, LTss and TNFR1 signaling. |
