Lymphocyte Proliferation in response to Cardiomyosin ex vivo

Document Type


Publication Date

Summer 2018

JAX Location

In: Student Reports, Summer 2018, The Jackson Laboratory


Following a myocardial infarction (MI), commonly known as a heart attack, there is significant scarring of the heart and a decrease of heart function. It has been hypothesized that an autoimmune response to cardiomyosin, a protein found in cardiac tissue, exacerbates the reactive fibrosis. Different mice strains' splenocytes were exposed to cardiomyosin in vitro and other control stimulants such as lymphocyte antibodies. Using flow cytometry, the proliferation of B- and T-lymphocytes was collected in the form of cell counts. The cell counts revealed that certain mice strains responded with greater lymphocyte proliferation when exposed to cardiomyosin, specifically the AJJ strain. This strain's splenocytes were tested again, using 2-deoxy-D-glucose (2-DG) at different dosages to measure if the response to cardiomyosin could be targeted. The cell counts revealed a decrease in lymphocyte proliferation to all stimulants across the board. The differing responses by the strains are most likely due to differences in their genomes, revealing that the autoimmune cardiomyosin response may have underlying genetic markers. This paves the way to a potential genetic therapy, an alternative to the pharmaceutical approach using 2-DG and other compounds.

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