Kidins220 and Aiolos promote thymic iNKT cell development by reducing TCR signals.

Development of T cells is controlled by the signal strength of the TCR. The scaffold protein kinase D-interacting substrate of 220 kilodalton (Kidins220) binds to the TCR; however, its role in T cell development was unknown. Here, we show that T cell-specific Kidins220 knockout (T-KO) mice have strongly reduced invariant natural killer T (iNKT) cell numbers and modest decreases in conventional T cells.

Kidins220 regulates the development of B cells bearing the λ light chain.

The ratio between κ and λ light chain (LC)-expressing B cells varies considerably between species. We recently identified Kinase D-interacting substrate of 220 kDa (Kidins220) as an interaction partner of the BCR. ablation of Kidins220 in B cells resulted in a marked reduction of λLC-expressing B cells.

Cross-TCR Antagonism Revealed by Optogenetically Tuning the Half-Life of the TCR Ligand Binding.

Activation of T cells by agonistic peptide-MHC can be inhibited by antagonistic ones. However, the exact mechanism remains elusive. We used Jurkat cells expressing two different TCRs and tested whether stimulation of the endogenous TCR by agonistic anti-Vβ8 antibodies can be modulated by ligand-binding to the second, optogenetic TCR.

Proximal Promoter-Driven Function Is Limited in Neonatal and Ineffective in Adult γδ T Cell Development.

During T cell development, gene expression is temporally controlled by its proximal and distal promoters. The transgenic mouse available from The Jackson Laboratory, in which the proximal promoter of drives expression, is a commonly used driver line to recombine genes flanked by sites in T cells. drives recombination early in thymocyte development and is frequently used to delete genes in αβ and γδ T cells.