Presentation Title

The Role of Glycogen Metabolism in B Cell Effector Function

Project Collaborators

Princess Rodriguez

Abstract

Upon activation, B cells increase their metabolic activity and have an increased demand for glucose. In the event that glucose is depleted, another source of energy must become available to meet the metabolic needs required for various effector functions including proliferation, antibody-secretion, and class-switching. We have previously shown that dendritic cells store glycogen for early effector cell activation. Here, we show that B-cells also express the enzymatic machinery required for glycogen metabolism. These include the two rate-limiting enzymes required for the synthesis and breakdown of glycogen, glycogen synthase (GYS) and glycogen phosphorylase (PYG), respectively. Upon chemical inhibition of PYG with CP-91149, we observed a decrease in both cell proliferation and antibody secretion. However, this dose of CP-91149 did not impact overall cell survival, therefore indicating that inhibition of PYG alone negatively impacted downstream effector functions of B-cells. In the future, we will be comparing the effects of GYS1 knockdown in B-cells using murine models to PYG pharmacological inhibition.

Primary Faculty Mentor Name

Eyal Amiel

Graduate Student Mentors

Princess Rodriguez

Status

Undergraduate

Student College

College of Agriculture and Life Sciences

Program/Major

Biochemistry

Primary Research Category

Biological Sciences

Secondary Research Category

Health Sciences

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The Role of Glycogen Metabolism in B Cell Effector Function

Upon activation, B cells increase their metabolic activity and have an increased demand for glucose. In the event that glucose is depleted, another source of energy must become available to meet the metabolic needs required for various effector functions including proliferation, antibody-secretion, and class-switching. We have previously shown that dendritic cells store glycogen for early effector cell activation. Here, we show that B-cells also express the enzymatic machinery required for glycogen metabolism. These include the two rate-limiting enzymes required for the synthesis and breakdown of glycogen, glycogen synthase (GYS) and glycogen phosphorylase (PYG), respectively. Upon chemical inhibition of PYG with CP-91149, we observed a decrease in both cell proliferation and antibody secretion. However, this dose of CP-91149 did not impact overall cell survival, therefore indicating that inhibition of PYG alone negatively impacted downstream effector functions of B-cells. In the future, we will be comparing the effects of GYS1 knockdown in B-cells using murine models to PYG pharmacological inhibition.