Sepsis leads to lasting changes in the composition of the pre-existing memory CD8 T cell compartment leading to altered localization, changes in their transcriptional landscape and chromatin accessibility, differential function, and reduced capacity to control infection.

Autophagy is required for CD8⁺ T cell memory formation; in aged individuals autophagy levels are diminished, and increasing autophagy enhances their CD8⁺ T cell responses.

Repeated antigen encounters alter the transcriptional state and function of lymph node-resident memory CD8⁺ T cells to mediate improved immunity against viral infection.

Immunological analysis of wild-type and Crlf2^-/- mice reveals a role for the cytokine thymic stromal lymphopoietin on memory CD8⁺ T-cell responses to viral infection, findings with potential translational implications.

CD8+ Trm cells' erosion role in oral lichen planus via IFN-γ, TNF-α, and IL17 cytokines has been revealed, addressing a gap in recurrent erosion studies.

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.

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.

Redundancy in the costimulatory signals that drive CD8⁺ T cell expansion is dictated by pathogen-specific cues.

Intercellular interactions between fibrocytes and CD8⁺ T lymphocytes promote inflammation through a pathophysiological positive feedback loop in bronchi of patients with chronic obstructive pulmonary disease (COPD).

Naïve CD8⁺ T cells are dysregulated during chronic hepatitis C (HCV) infection, and this is reversible after viral clearance.