Loss of hepatic Cdk1 leads to oxidative stress, increased fatty acids in blood, and hyperinsulinemia, which resulted in insulin resistance and hepatic steatosis, similar as in diabetes.

Identification and characterisation of proteins and processes regulated by HIV in primary human CD4+ T cells using an HIV reporter virus for one-step, antibody-free magnetic selection.

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.

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

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

A new potent and selective CDK9 inhibitor induces the expression of the proto-oncogene MYC via a mechanism that depends on the bromodomain protein BRD4.

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.

Sepsis-induced numerical loss of naive autoantigen-specific CD4 T cells reduces host capacity to develop autoimmune immune disease, thereby demonstrating an intriguing relationship between infection and autoimmune disease.

Behaviorally-driven expression of the immediate early gene transcription factor NPAS4 changes local circuit connectivity and short-term plasticity by selectively recruiting CCK basket cell synapses to pyramidal neuron somas.

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.