| First Author | Hundt M | Year | 2006 |
| Journal | Immunity | Volume | 24 |
| Issue | 5 | Pages | 513-22 |
| PubMed ID | 16713970 | Mgi Jnum | J:113357 |
| Mgi Id | MGI:3665511 | Doi | 10.1016/j.immuni.2006.03.011 |
| Citation | Hundt M, et al. (2006) Impaired activation and localization of LAT in anergic T cells as a consequence of a selective palmitoylation defect. Immunity 24(5):513-22 |
| abstractText | The molecular basis of T cell anergy is not completely understood. We show that in antigen-primed anergic murine CD4(+) T cells the linker for activation of T cells (LAT) is hypophosphorylated upon CD3/CD28 restimulation. Signaling events downstream of LAT (PLCgamma1 phosphorylation and p85 [PI3-K] association) were impaired, whereas upstream events (CD3zeta and ZAP-70 phosphorylation) remained intact. LAT recruitment to the immunological synapse and its localization in detergent-resistant membrane (DRM) fractions were defective in anergic T cells. These defects resulted from impaired palmitoylation of LAT and were selective since the DRM localization and palmitoylation of Fyn were intact. This LAT defect was independent of Cbl-b and did not reflect enhanced LAT degradation. These results identify LAT as the most upstream target of anergy induction; moreover, they suggest that regulation of the amount of LAT in the immunological synapse and DRM by posttranslational palmitoylation contributes to the induction of T cell anergy. |
