Determining Whether the Protein Tyrosine Phosphatase Non-Receptor Type 2 (PTPN2) Gene Plays a Role in the Development of Type 1 Diabetes

Overview

Type 1 diabetes (T1D) is an autoimmune disease that leads to destruction of insulin producing 𝛽-cells. It is unknown what causes the disease and there’s no lasting cure. The protein tyrosine phosphatase non - receptor type2 (PTPN2) gene may play an important role in the disease. Mutations in the gene are often associated with increased risk of TID development. However, it is unclear what role PTPN2 plays in regulating antibody producing B-cells, and how it subsequently affects immune regulation. If PTPN2 plays a role in regulating B-cell antibody production, it was hypothesized that antibody production will increase if PTPN2 is deleted. Our study explores how PTPN2 deletion affects total IgG and IgG isotype antibody production in B-cells using the enzyme linked immunosorbent assay (ELISA). Our experiments compared the antibody levels of mice with PTPN2 knockout/deletion (PTPN2-KO) in their B-cells and control/wild-type (WT) mice with normal PTPN2 expression. There was, on average, a 48.332% increase in total IgG antibodies in PTPN2 -KOs compared to WTs. There was also a trend towards increase in IgG isotypes: IgG1, IgG2a, IgG2b with percent increases of 30.17%, 11.459% and 16.23% respectively in PTPN2 -KO mice. There wasn’t a significant change in IgG3 antibody levels. The increase in total IgG antibodies was proven statistically significant. These results suggest that PTPN2 in B -cells plays an important role in regulating total IgG antibody production and its deletion may contribute to the development of T1D. This finding may help in developing gene therapy as a T1D solution.

Competition history

• JSHS 2024 Category not listed

Resources

• National JSHS abstract book ↗

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