Proliferation and differentiation of CD8⁺ T cells into terminal effectors occurs in the marginal zone and red pulp, and is promoted by IL-12 through direct and indirect mechanisms.

Pathogen-specific CTLs are programmed to provide customized responses against infection, by inflammatory molecules that promote localization in peripheral and lymphoid tissues using alternative signaling mechanisms.

TCR-mediated downregulation of let-7 microRNAs licenses the differentiation of activated CD8 T cells into cytotoxic T lymphocytes.

The acquisition of cytotoxic function by human CD4 T cells is an integral part of the T helper 1 differentiation pathway and is limited by the transcription factor ThPOK.

The interplay between the cytokine TGFβ and the PD-1/PD-L1 pathway promotes CD8+ T cell anergy and tolerance towards transplanted tissues.

PDK1 serves as a critical role for intrinsically promoting T follicular helper cell differentiation and effector functions via controlling expression level of TCF1.

Deficiency of the transcriptional repressor, Bach2, results in more mature mouse natural killer cells.

PLWH over a decade of ART showed a significant reshaping of the function and expression of inhibitory receptors across the CD8+ T cell landscape, ultimately leading to a decrease of CD107a TIGIT HIV-1-specific CD8+ T cells recovered by TIGIT blockade.

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.

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