Assessing B Cell Differentiation Following Asbestos Fiber Exposure

Additional Funding Sources

The funding for this project was supported or partially supported by a 2018-2019 STEM Undergraduate Research Grant from the Higher Education Research Council.

Presentation Date

7-2019

Abstract

B cells are the main pathogenesis drivers in autoimmune diseases. Subtypes of B cells, known as B regulatory (Breg) or B10 cells contain a suppressive function, which down regulates the immune response. This is primarily conducted by IL-10, which is an inhibitory cytokine that is produced by the B10 subset. Recent evidence indicates that exposure to different asbestos fiber cause the activation of the immune system, however there is a difference in the response created by each fiber type. The Libby amphibole (LA) fiber leads to autoimmune response, whereas Chrysotile (Chry) fiber exposure does not. We hypothesize that this difference occurs because Chry exposure increases the production of B10 cell to keep the immune system suppressed. To test this, we will collect mouse splenocytes and expose the cells to the different asbestos fibers for 48 or 96 hours. As a control, the splenocytes will be exposed to the proteins, BAFF or IL-21. These proteins have been shown to stimulate proliferation of B10 cells. Next, we will use antibodies against cell surface markers and flow cytometry in order to identify B cell subtypes. Thus, we can investigate B cell differentiation, with the hypothesis that LA will decrease Breg differentiation, whereas Chry will increase Breg differentiation. This investigation will increase our understanding of how different asbestos fibers induce Breg production.

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Assessing B Cell Differentiation Following Asbestos Fiber Exposure

B cells are the main pathogenesis drivers in autoimmune diseases. Subtypes of B cells, known as B regulatory (Breg) or B10 cells contain a suppressive function, which down regulates the immune response. This is primarily conducted by IL-10, which is an inhibitory cytokine that is produced by the B10 subset. Recent evidence indicates that exposure to different asbestos fiber cause the activation of the immune system, however there is a difference in the response created by each fiber type. The Libby amphibole (LA) fiber leads to autoimmune response, whereas Chrysotile (Chry) fiber exposure does not. We hypothesize that this difference occurs because Chry exposure increases the production of B10 cell to keep the immune system suppressed. To test this, we will collect mouse splenocytes and expose the cells to the different asbestos fibers for 48 or 96 hours. As a control, the splenocytes will be exposed to the proteins, BAFF or IL-21. These proteins have been shown to stimulate proliferation of B10 cells. Next, we will use antibodies against cell surface markers and flow cytometry in order to identify B cell subtypes. Thus, we can investigate B cell differentiation, with the hypothesis that LA will decrease Breg differentiation, whereas Chry will increase Breg differentiation. This investigation will increase our understanding of how different asbestos fibers induce Breg production.