GAD65 (206-220)

Product Name: GAD65 (206-220)

Sequence One Letter Code: TYEIAPVFVLLEYVT

Sequence Three Letter Code: H-Thr-Tyr-Glu-Ile-Ala-Pro-Val-Phe-Val-Leu-Leu-Glu-Tyr-Val-Thr-OH

Chemical Formula:C86H129N15O24

Molecular Weight: 1757.2

Purity: 95%

Form: Lyophilized

Storage Conditions: - 20 °C

Research Area: Inflammation and Immunology Research

Source / Species: human, mouse, rat, bovine, pig

Conjugation: Unconjugated

Code Nacres: NA.26

Application: GAD65 (206–220) is a synthetic peptide corresponding to residues 206–220 of glutamic acid decarboxylase 65 (GAD65), a major autoantigen in autoimmune diabetes. Presented by I-Ag7 MHC class II molecules to CD4⁺ T cells, this epitope plays a significant role in antigen-specific immune responses associated with type 1 diabetes. The peptide is widely used to investigate T cell activation, immune tolerance mechanisms, and autoimmune pathogenesis. It has also been incorporated into Ig chimeric constructs to study regulatory pathways, including interleukin-10–mediated modulation of CTLA-4 expression. GAD65 (206–220) supports experimental models focused on antigen presentation, T cell–mediated autoimmunity, and therapeutic strategies targeting immune regulation in diabetes research.

Current Research: GAD65 (206–220) is a synthetic peptide corresponding to amino acid residues 206–220 of glutamic acid decarboxylase 65 (GAD65), one of the principal autoantigens implicated in type 1 diabetes (T1D). GAD65 is an enzyme responsible for catalyzing the conversion of glutamate to γ-aminobutyric acid (GABA) and is expressed in pancreatic β cells as well as in neurons. In the context of autoimmune diabetes, GAD65 becomes a target of autoreactive T cell and antibody responses, contributing to immune-mediated destruction of insulin-producing β cells. The 206–220 epitope is presented by the diabetes-associated MHC class II molecule I-A^g7 in non-obese diabetic (NOD) mice, a widely used model of spontaneous autoimmune diabetes. Upon antigen processing, this peptide binds to I-A^g7 and is recognized by CD4⁺ T helper cells, driving antigen-specific immune responses that contribute to pancreatic islet inflammation (insulitis). The defined nature of this epitope allows precise analysis of T cell receptor (TCR) specificity, peptide–MHC binding stability, and clonal expansion of autoreactive CD4⁺ T cells. Functionally, GAD65 (206–220) is used to stimulate antigen-specific CD4⁺ T cells in vitro and in vivo. Assays commonly include T cell proliferation measurements, cytokine profiling (e.g., IFN-γ, IL-2, IL-17), and flow cytometric analysis of activation markers. The peptide enables detailed examination of Th1- and Th17-associated inflammatory pathways that are implicated in β cell destruction. In addition, regulatory T cell (Treg) responses specific to this epitope can be assessed, providing insight into tolerance mechanisms that normally prevent autoimmunity. A major area of investigation involving GAD65 (206–220) concerns immune tolerance and immunomodulation strategies. Because T1D results from breakdown of peripheral tolerance to β cell antigens, this peptide has been incorporated into tolerogenic vaccine approaches, antigen-coupled cell therapies, and Ig chimeric constructs designed to promote immune regulation. Fusion of GAD65 epitopes to immunoglobulin scaffolds has been used to enhance antigen presentation under tolerogenic conditions, facilitating induction of regulatory pathways. In particular, interleukin-10 (IL-10)–dependent mechanisms and modulation of CTLA-4 expression have been explored in peptide-based interventions aimed at suppressing autoreactive T cell responses. GAD65 (206–220) is also applied in studies of antigen processing and epitope hierarchy. Investigators examine how peptide affinity for I-A^g7 influences immunodominance and T cell selection in the thymus and periphery. Altered peptide ligands derived from the 206–220 sequence are frequently used to probe TCR signaling thresholds, partial agonism, and mechanisms of anergy induction. In translational diabetes research, the peptide supports evaluation of immunotherapeutic strategies such as costimulatory blockade, cytokine modulation, nanoparticle-based antigen delivery, and cell-based tolerance induction. Because disease progression in NOD mice can be monitored longitudinally, the impact of antigen-specific interventions targeting GAD65 (206–220) can be quantitatively assessed through glycemic measurements, insulitis scoring, and immune phenotyping. Overall, GAD65 (206–220) is a well-characterized MHC class II–restricted autoantigenic epitope central to experimental models of type 1 diabetes. Its defined immunological properties make it an essential tool for dissecting CD4⁺ T cell activation, antigen presentation dynamics, immune tolerance mechanisms, and therapeutic approaches aimed at restoring immune regulation in autoimmune diabetes.