| First Author | Prlic M | Year | 2011 |
| Journal | J Immunol | Volume | 187 |
| Issue | 4 | Pages | 1542-6 |
| PubMed ID | 21724993 | Mgi Jnum | J:179176 |
| Mgi Id | MGI:5301233 | Doi | 10.4049/jimmunol.1100907 |
| Citation | Prlic M, et al. (2011) Cutting edge: beta-catenin is dispensable for T cell effector differentiation, memory formation, and recall responses. J Immunol 187(4):1542-6 |
| abstractText | The molecular mechanisms that regulate mature T cell fate and enable cells to differentiate into memory T cells are largely unknown. Memory T cells share certain key features with stem cells: they both have the ability to self-renew and are long-lived. The Wnt-beta-catenin signaling pathway is a key player in regulating stem cell self-renewal and differentiation. We generated a conditional knockout mouse that specifically lacks beta-catenin in mature T cells and report in this article that beta-catenin is not involved in regulating effector versus memory T cell differentiation. beta-catenin-deficient memory T cells were phenotypically and functionally indistinguishable from control cells and made normal recall responses. beta-catenin deficiency does not affect T cell migration, T cell function in a model of chronic infection, or lymphopenia-induced proliferation. Together, our data suggest that self-renewal and differentiation are regulated differently in memory T cells compared with epithelial and hematopoietic stem cells. |
