Transient Depletion of Foxp3⁺ Regulatory T Cells Selectively Promotes Aggressive β Cell Autoimmunity in Genetically Susceptible DEREG Mice.

ABSTRACT: Type 1 diabetes (T1D) represents a hallmark of the fatal multiorgan autoimmune syndrome affecting humans with abrogated Foxp3⁺ regulatory T (Treg) cell function due to Foxp3 gene mutations, but whether the loss of Foxp3⁺ Treg cell activity is indeed sufficient to promote β cell autoimmunity requires further scrutiny. As opposed to human Treg cell deficiency, β cell autoimmunity has not been observed in non-autoimmune-prone mice with constitutive Foxp3 deficiency or after diphtheria toxin receptor (DTR)-mediated ablation of Foxp3⁺ Treg cells. In the spontaneous nonobese diabetic (NOD) mouse model of T1D, constitutive Foxp3 deficiency did not result in invasive insulitis and hyperglycemia, and previous studies on Foxp3⁺ Treg cell abla

SUBMITTER: Watts D 

PROVIDER: S-EPMC8382961 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature