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The Washington Research Foundation Fellowship
Alevtina Gall, Cell and Molecular Biology & International Studies - 2007-08 RFAU
Tina first got involved in research in 2004 when she worked on the Jury and Democracy project with Dr. John Gastil in the Department of Communication. After having a very positive first research experience she decided to follow her interests and seek out research opportunities in the biological sciences. Tina discovered her passion for immunology and infectious diseases while working under the supervision of Dr. Martin Holland at the Medical Research Council in The Gambia, West Africa. She spent five months in The Gambia studying the immune responses of patients who had previously been infected with the ocular strain of Chlamydia trachomatis. Once she returned to Seattle, she joined Dr. Kevin Urdahl’s team and began working on a project looking at the role of a specific subset of immune cells in infection with Mycobacterium tuberculosis. Tina attributes her undergraduate research success to having the opportunity to work with incredibly inspiring and encouraging mentors, all of whom pushed her to become a better critical thinker and scientist. In the future, Tina hopes to combine her passion for immunology research and international health by pursuing an MD/PhD degree and apply her skills toward serving neglected communities in the United States and abroad.
Mentor: Dr. Kevin Urdahl, Pediatrics
Project Title: The role of regulatory T cells in Mycobacterium Tuberculosis infection
Abstract: Tuberculosis is a disease that annually kills two million people, predominantly those living in developing countries. Bacillus Calmette-Guerin (BCG), the currently used vaccine against tuberculosis, is not effective in geographical areas with the highest disease burden. The ability of Mycobacterium tuberculosis (Mtb) to establish a persistent infection may depend on a mechanism used by the pathogen to circumvent the natural immune response of the host. Regulatory T cells (Tregs), a subset of Foxp3-expressing CD4 + T cells, provide a “self-check” mechanism to prevent autoimmunity and play an important role in moderating the anti-microbial response of the host. We hypothesize that pathogen-specific regulatory T cells are activated during M. tuberculosis infection and suppress the proinflammatory response of the host that may otherwise be sufficient to clear the infection. My project focuses on designing an in vitro model to test our hypothesis that Mtb-specific regulatory T cells are induced during tuberculosis. Currently we are using bone-marrow derived dendritic cells (BMDCs) infected with Mtb to compare the proliferative capacity of regulatory T cells isolated from Mtb-infected and uninfected mice. We hypothesize that regulatory T cells from mice with tuberculosis will show high levels of proliferation in response to Mtb antigens presented by infected BMDCs. Using a complementary strategy, we will test whether Tregs from Mtb-infected mice are specific for an immunodominant Mtb-derived antigen using MHC class II tetramers. Understanding the role of Mtb-specific T regs in regulating immunity in tuberculosis has the potential to inform new strategies for designing an effective vaccine, and novel therapies for treating multi-drug resistant tuberculosis.