We examined the frequency and phenotype of circulating preproinsulin (PPI)-specific and insulin B (InsB)-specific CD8<sup>+</sup> T cells in HLA-B*3906<sup>+</sup> children newly diagnosed with T1D and in high-risk HLA-A*2402<sup>+</sup> children before the appearance of disease-specific autoantibodies and before diagnosis of T1D.
Compared to healthy controls, B10 cell percentages in T1D were significantly lower (5.6±3.5% vs. 6.9±3.3%; P <0.05), produced less IL-10 (15.4±4.3% vs. 29.0±4.5%; P <0.001), and lacked regulatory capacity.
This vaccine immunized into prediabetic NOD mice subcutaneously could induce IL-10 and TGF-β expressing pTregs and lead to suppressing autoreactive T cells responses, resulting in the prevention of T1D in these animals.
Among 52 participants whose human leukocyte antigen typing was carried out, all of the participants with slowly progressive insulin-dependent diabetes mellitus who had DRB1*09:01 were positive by GADA-ELISA (P = 0.021).
We previously reported that Clec16a deficiency modified immune reactivity and protected against autoimmunity in the nonobese diabetic (NOD) mouse model for T1D.
IGF1 and IGF2 showed longitudinal stability in single AAb+ subjects, but IGF1 levels decreased over time in subjects with multiple AAb and those who progressed to type 1 diabetes, particularly post-diagnosis.
The combination of QIV and LGG reduced inflammatory responses (i.e., IFN-γ, IL17A, IL-17F, IL-6, and TNF-α) from activated PBMCs of pediatric patients with T1D, without dampening the production of seroprotective antibodies.
IGF1 and IGF2 showed longitudinal stability in single AAb+ subjects, but IGF1 levels decreased over time in subjects with multiple AAb and those who progressed to type 1 diabetes, particularly post-diagnosis.
We examined the frequency and phenotype of circulating preproinsulin (PPI)-specific and insulin B (InsB)-specific CD8<sup>+</sup> T cells in HLA-B*3906<sup>+</sup> children newly diagnosed with T1D and in high-risk HLA-A*2402<sup>+</sup> children before the appearance of disease-specific autoantibodies and before diagnosis of T1D.
We report two patients with biallelic functionally null variants of the NEUROG3 gene who nonetheless did not present with IDDM during infancy, but instead developed permanent IDDM during middle childhood ages.
This vaccine immunized into prediabetic NOD mice subcutaneously could induce IL-10 and TGF-β expressing pTregs and lead to suppressing autoreactive T cells responses, resulting in the prevention of T1D in these animals.
The present article describes the effect on glucose of small doses of subcutaneous glucagon to revert hypoglycemia and prevent severe events in small children with type 1 diabetes using a continuous glucose monitoring.
In this article we have used consensus expert opinion alongside the available evidence, product indication and most recent clinical guidance to provide support for the diabetes healthcare community regarding the appropriate use of SGLT2 inhibitors, focussing on specific considerations for appropriate prescribing of dapagliflozin within the T1DM management pathway.
A physician-initiated double-blind, randomised, placebo-controlled, phase 2 study evaluating the efficacy and safety of inhibition of NADPH oxidase with the first-in-class Nox-1/4 inhibitor, GKT137831, in adults with type 1 diabetes and persistently elevated urinary albumin excretion: protocol and statistical considerations.
We studied these issues by expressing human AIRE (huAIRE) as a modifier of tolerance function in NOD mice wherein the defects of thymic and peripheral tolerance together cause type I diabetes (T1D).
We investigated associations of antibodies against the 65 kDa isoform of GAD (GAD65) with type 1 diabetes and type 2 diabetes genetic risk scores and incident diabetes in adults in European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct, a case-cohort study nested in the EPIC cohort.