Development of mouse thymocytes through the pre-TCR checkpoint requires WNK1 kinase signalling via the OXSR1 and STK39 kinases and the SLC12A2 ion co-transporter leading to MYC-dependent cell proliferation.

Endoplasmic reticulum-associated degradation (ERAD) is a critical protein quality control checkpoint for thymocyte β-slection.

Two-photon microscopy, combined with chemotaxis assays, synchronized thymocyte selection studies, and flow cytometry analyses, reveal that CCR4 and CCR7 promote medullary entry and central tolerance of immature and mature post-positive selection thymocyte subsets, respectively, with distinct outcomes for central tolerance.

CD4 lineage commitment requires HDAC3 to prevent premature upregulation of CD8 lineage genes during T cell development.

Self-reactive thymocyte death is most efficient when peptide-presenting cells are phagocytic, and blocking phagocytosis inhibits self-reactive thymocyte death, suggesting that phagocytes play central roles during thymocyte negative selection.

The p21-activated kinase 2 (Pak2) is an essential regulator that governs the actin cytoskeleton-dependent signaling to ensure normal thymocyte development, maturation and egress.

Antagonistic signaling by the kinases PI3K and Itpkb limits the kinetics and enforces the Notch-dependence of beta-selection – the most important cell-fate determining process in alpha beta T cell development.

Genetically modified mouse model and comprehensive analysis reveal the molecular mechanisms regulating early T-cell development through intracellular TCRβ expression-mediated β-selection and independent cell survival signaling.

Fam49b is a critical regulator of selection process to ensure normal thymocyte development and peripheral T cells survival.

A novel zinc finger transcription factor regulates expression of multiple genes in late stage thymocytes and recent thymic emigrants to promote formation of the naïve T cell compartment.