Calcium-calcineurin signaling cascade drives the acquisition of both the phenotype of the most self-reactive naive CD4 T cells and their enhanced cell-intrinsic ability to commit into induced regulatory T cells upon activation.

Higher affinity for self-pMHC complexes and broader promiscuity for foreign-pMHC complexes imparts a fitness advantage within the CD4⁺ T cell compartment in older mice.

High-throughput sequencing of the memory T cell receptor repertoire and machine learning can predict robust antibody and CD4 T cell response to de novo hepatitis B vaccine.

Inflamasomme inhibition prevents immune activation, HIV-1 pathogenesis and the splenic content of HIV-1 total DNA in humanized mice when administrated early after HIV-1 infection.

Histone deacetylase 3 is required for CD4+ T cells to downregulate two cholesterol efflux transport proteins, ABCA1 and ABCG1, for successful proliferation after antigenic stimulation.

Cytotoxic CD4 T lymphocytes are abundantly generated in T. cruzi-infected mice, predominantly infiltrate infected hearts, depend on T-cell intrinsic IL-18R/MyD88 signaling for expansion and their blood frequency correlates with the severity of chronic myocarditis in patients with Chagas disease.

The results presented here indicate that IL-10-producing CD4⁺ T cells express genes associated with chronically activated T_H1-like cells, undergo clonal expansion, and inhibit antiviral T cell responses via the secretion of arginase-1, facilitating viral persistence in mice infected with MCMV.

Eutherian CD4 evolved counterbalancing motifs in the extracellular, transmembrane, and intracellular domains that regulate CD4⁺ T cell responses to peptide antigens presented by class II MHC (pMHCII).

Phenotypic diversity and cell state transition (i.e., acquisition of a CD44+/CD24- cell state or exposure to TGF-beta) can spur intra-tumor genetic heterogeneity and contribute to acquired resistance.

Description of the transcriptional and clonal landscape of virus-specific CD4⁺ T cells in acute and chronic viral infections, and a new reference map to interpret CD4 T cell diversity across tissues and biological models.