The metabolic hormone leptin promotes the function of T FH cells and supports vaccine responses. Circulating T FH cells, serological memory, and tissue compartmentalization shape human influenza-specific B cell immunity.

Induction of ICOS +CXCR3 +CXCR5 + T H cells correlates with antibody responses to influenza vaccination. Follicular helper T cell profiles predict response to costimulation blockade in type 1 diabetes. Low-dose interleukin-2 treatment selectively modulates CD4( +) T cell subsets in patients with systemic lupus erythematosus. T follicular helper cells and T follicular regulatory cells in rheumatic diseases. Follicular helper cell biology: a decade of discovery and diseases. Our findings reveal the central role of the selenium–GPX4–ferroptosis axis in regulating T FH homeostasis, which can be targeted to enhance T FH cell function in infection and following vaccination.

Selenium supplementation enhanced GPX4 expression in T cells, increased T FH cell numbers and promoted antibody responses in immunized mice and young adults after influenza vaccination. The deletion of GPX4 in T cells selectively abrogated T FH cells and germinal center responses in immunized mice. Glutathione peroxidase 4 (GPX4) is the major lipid peroxidation scavenger and is necessary for T FH cell survival. Here we report that T FH cells show intensified lipid peroxidation and altered mitochondrial morphology, resembling the features of ferroptosis, a form of programmed cell death that is driven by iron-dependent accumulation of lipid peroxidation.

The regulation of T FH cell survival remains unclear. Nature Immunology volume 22, pages 1127–1139 ( 2021) Cite this articleįollicular helper T (T FH) cells are a specialized subset of CD4 + T cells that essentially support germinal center responses where high-affinity and long-lived humoral immunity is generated. Selenium–GPX4 axis protects follicular helper T cells from ferroptosis

Selenium following axis