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.

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

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.

The cytotoxicity exerted by CD8⁺ T cells against parasitized erythroblasts helps to protect against blood-stage malaria by making parasitized cells susceptible to phagocytosis.

HLA-B*35:01 molecules that are peptide-deficient are thermostable, bind CD8 with higher affinity than their peptide-filled versions, accumulate at immunological synapses and enhance antigen-specific CD8+ T cell immune responses.

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

The thymic selection of the human T-cell receptor repertoire releases polyspecific receptors with the ability to recognize and respond to peptides from unrelated viruses.

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).

Regulatory T cell suppress cytotoxic T cells in autoimmunity and cancer by taking up IL-2.

Identification and characterization of the responses of T lymphocytes that are specific for 'self' tissue antigens, revealing the functional limits of immune tolerance.