Romain Bedel

TL;DR: Natural killer T cells (NKT cells) constitute a distinct subset of T lymphocytes that can modulate immune responses through the rapid release of cytokines and direct interactions with other cells of the immune system and are promising targets for immunotherapy.

TL;DR: It is shown, by analysing mice carrying mutant Zap70 genes, that T cell receptor signaling strength induces epigenetic changes of genes to modulate iNKT lineages, suggesting that variable TCR signaling modulates regulatory element activity at NFAT and Egr binding sites exerting a determinative influence on the dynamics of gene enhancer accessibility and the developmental fate of iN KT cells.

TL;DR: It is shown that there is a greater interplay between the germline– and nongermline–encoded loops within the TCR β-chain of the Vβ2 NKT TCR that enables CD1d-Ag ligation.

TL;DR: Proper development of fully functional iNKT cells is constrained by a limited range of TCR affinity that plays a key role in triggering the iN KT cell-differentiation pathway.

TL;DR: A new NKT-deficient mouse strain is created using transcription activator-like effector nuclease (TALEN) technology to only disrupt the expression of Jα18, leaving the remaining Jα repertoire unperturbed and serving as a new model of iNKT cell deficiency.