Finally, we show that B cells in NOD mice express reduced PTEN, and low-dosage p110δ inhibitor therapy blocks disease progression in this model of type 1 diabetes.
Antibodies to glutamic acid decarboxylase (GAD65 [GADA]) and the intracellular portion of protein tyrosine phosphatase (IA-2(ic) [IA-2A]) were measured by similar, but not identical, methods in samples from participants in the Type 1 Diabetes Genetics Consortium (T1DGC).
The R620W polymorphism in the protein-tyrosine-phosphatase nonreceptor type 22 gene (PTPN22) confers susceptibility to type 1 diabetes (T1D) and other autoimmune diseases.
In a registry-based group of 525 recent-onset IDDM patients <40 years old we investigated the possible interactions of a CTLA-4 gene A-to-G transition polymorphism with age at clinical disease onset and with the presence or absence of established genetic (HLA-DQ, INS VNTR) and immune disease markers (autoantibodies against islet cell cytoplasm (ICA); insulin (IAA); glutamate decarboxylase (GAD65-Ab); IA-2 protein tyrosine phosphatase (IA-2-Ab)) determined within the first week of insulin treatment.In new-onset IDDM patients.
Cloning and characterization of islet cell antigen-related protein-tyrosine phosphatase (PTP), a novel receptor-like PTP and autoantigen in insulin-dependent diabetes.
However, we did find interactions between GM, HLA-DR, and Type 1 diabetes (significant or of borderline significance after considering the effect of multiple tests): possession of Glm(2) appeared to increase susceptibility to diabetes in individuals who had HLA-DR3 but not HLA-DR4, while possession of G3m(5) appeared to increase susceptibility in individuals who had HLA-DR4 but not HLA-DR3.