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Lu, Julia Chi Lam

University of British Columbia

Innate lymphoid cells (ILCs) are a rare population of innate immune cells that are part of the first line of defense against pathogens. These cells arise from the same lymphoid lineage that B cells, T cells, and NK cells belong to. Type 2 ILCs (ILC2s) are a subset of ILCs that reside in the lungs, mucosal layers, and skin, and have roles in clearing helminth infections, triggering allergic responses, and promoting lung tissue repair after Influenza infections. The function of these cells mirrors those of TH2 cells but lack the ability to recognize antigens. However, their full developmental background is still unknown. It is currently understood that ILC2s develop in the fetal liver and adult bone marrow from common lymphoid progenitors and differentiate into several intermediates before being classified as ILC2 progenitors (ILC2p). ILC2ps express interleukin-7 (IL-7) receptor with the aid of the transcription factor GATA3. Our lab has shown that IL-7 is a critical growth factor for ILC2 development as mutations to the IL-7 receptor showed a reduction in the ILC2 population and GATA-3 expression. Conversely, overexpression of IL-7 resulted in the expansion of the ILC2 population and elevated GATA-3 expression. I hypothesized that IL-7 transcriptionally regulates ILC2 maintenance and immune responses. Using qRT-PCR and high-parameter flow cytometry, I examined ILC2 development dependence on IL-7 and maternal IL-7 influence on offspring ILC2 populations. Through RNA sequencing, I identified the differences in the transcriptional landscapes regulated by IL-7 and thymic stromal lymphopoietin (TSLP) in lung ILC2s. This body of work will not only increase our understanding of a rare but vital cell population, but also contribute novel targets in therapeutic strategies for allergic asthma and viral infections.

Text

2022-08-19

Attribution-NonCommercial-NoDerivatives 4.0 International

http://hdl.handle.net/2429/82430

Microbiology and Immunology

University of British Columbia

UBCV

http://creativecommons.org/licenses/by-nc-nd/4.0/