| First Author | Mujal AM | Year | 2016 |
| Journal | Nat Immunol | Volume | 17 |
| Issue | 3 | Pages | 315-22 |
| PubMed ID | 26692174 | Mgi Jnum | J:258596 |
| Mgi Id | MGI:6141159 | Doi | 10.1038/ni.3330 |
| Citation | Mujal AM, et al. (2016) A septin requirement differentiates autonomous and contact-facilitated T cell proliferation. Nat Immunol 17(3):315-22 |
| abstractText | T cell proliferation is initiated by T cell antigen receptor (TCR) triggering, soluble growth factors or both. In characterizing T cells lacking the septin cytoskeleton, we found that successful cell division has discrete septin-dependent and septin-independent pathways. Septin-deficient T cells failed to complete cytokinesis when prompted by pharmacological activation or cytokines. In contrast, cell division was not dependent on septins when cell-cell contacts, such as those with antigen-presenting cells, provided a niche. This septin-independent pathway was mediated by phosphatidylinositol-3-OH kinase activation through a combination of integrins and costimulatory signals. We were able to differentiate between cytokine- and antigen-driven expansion in vivo and thus show that targeting septins has strong potential to moderate detrimental bystander or homeostatic cytokine-driven proliferation without influencing expansion driven by conventional antigen-presentation. |
