May 15, 2023 · Iron deficiencies in Treg caused by the depletion of Transferrin receptor 1, a major iron transporter, result in the abrogation of Treg in the intestine and lethal autoimmune disease.

Mar 19, 2025 · Iron metabolism and mitochondrial dynamics are among the key factors influencing Treg function. This review focuses on how iron and mitochondrial metabolism shape Treg biology and function.

Feb 28, 2022 · Here we showed that iron deficiency promotes Treg cell expansion by reducing ROS accumulation, improving the disease progression of pristane-induced lupus. Increased oxidative stress inhibits Treg cell differentiation by inducing cell apoptosis.

Mar 3, 2025 · Iron promotes ROS formation through Fenton reactions, and excessive iron accumulation can exacerbate oxidative stress and lipid peroxidation in Treg. This mechanism of ferroptosis could be targeted to prevent age-related disease.

Nov 15, 2013 · These data suggest that iron overload changes the balance of Treg and Th17 cells through the proliferation and activation of macrophages, and thereby effects on the immunological condition of some disease, such as GVHD and autoimmune.

Here we show that homeostasis of regulatory T cells in the intestine was dependent on high cellular iron levels, which were fostered by pentanoate, a short-chain fatty acid produced by intestinal...

In the pristane-induced lupus mouse model, insufficient iron promoted the expansion of Treg cells and reshaped the Th17/Treg cell balance, leading to remission of renal damage and the lower level of autoimmune antibodies in pristane-induced lupus.

Strong experimental evidence highlights the profound impact of metabolism on Treg. Their anti-in ammatory function and ability to suppress excessive immune responses. depend on the integration of metabolic cues with their transcriptional and signaling networks.

Mar 5, 2025 · Iron supplementation was associated with increased Tregs, further mitigating the immune responses in experimental cerebral malaria. 122 Tregs with 3-phosphoinositide-dependent protein kinase 1 deletion disrupt the iron balance by modulating MEK‒ERK signalling and TFR1 expression, which causes glucose metabolism inhibition but excessive ROS ...

Our data suggest that perinatal Tregs may exploit iron consumption as a means to favor gut colonization by beneficial bacteria early after birth. Supporting this idea, the hepcidin rise in cKO mice may be secondary to a very early increase in circulating iron.