Karl was a research technician in the Lab and received his B.S. in Biochemistry at Temple University in 2016. Before committing to a Ph.D program, Karl wanted more laboratory and research experience in order to make a final decision on what discipline he wants to focus on. Karl’s work included generating recombinant DNA and Protein, and performing immunofluorescence tissue staining using microscopy to help better understand the role of LINGOs and Trefoil Factors in the context of Type 2 immunity during helminth infection. In addition, Karl worked on a preeminent project that involves elucidating the role of the alarmin cytokine IL-33 in professional APC’s during Th2 driven immune responses.
Karl is currently a Ph.D. candidate at Thomas Jefferson University in the Biochemistry and Molecular Pharmacology program.
Where are you from?
What is your favorite hangout place or favorite thing to do?
I enjoy reading, listening to music, and working out!
What is your prior degree/training?
I received a B.S. in Biochemistry from Temple University and have both molecular biology and computational biology undergraduate experience. I have also learned how to program in Python and Bash (Ubuntu Terminal).
What is your career aspiration?
I am currently applying for PhD programs in Biochemistry, Bioengineering, and Bioinformatics. After obtaining my doctorate, I would like to manage projects and enter leadership roles in industry for research on drug design.
Updates on My Projects
Recent experiments of mine show a host protective phenotype upon infection with the GI parasitic nematodes Nippostrongylus brasiliensis and Heligmosomoides polygyrus in mice lacking professional APC derived IL-33. This result was unexpected because of two reasons; One because IL-33 is known to promote Type 2 immunity by acting on ST2+ ILC2s and Th2 Cells to produce the Type 2 Cytokine IL-4, IL-5, and IL-13 which constitute the primary inflammatory response against helminth infection. Two because there is contention on the question of biological relevance for the role of IL-33 derived from hematopoietic cells. My current data suggests that a defect in FOXP3+ T Regulatory cells in mice lacking IL-33 in professional APCs is contributing to an enhanced immune response.