Abstract/Description/Artist Statement
Regulatory T cells (Tregs) are central to immune tolerance, and their lineage stability is established during thymic development and maintained in the periphery through tightly regulated signaling networks. Members of the BMP receptor family have been implicated in T-cell differentiation, yet the specific role of the type I receptor ALK2 in shaping cell fate and sustaining the regulatory program remains unclear. To examine how ALK2 contributes to T-cell development, we generated ALK2-knockout murine chimeras and analyzed lymphoid populations from the thymus, spleen, and peripheral tissues. Thymocytes and lymphocytes were isolated and stained with antibody panels to identify developmental subsets and regulatory populations. Samples were analyzed by flow cytometry to determine whether disruption of ALK2 signaling alters thymic selection, or CD4⁺ lineage commitment. Early observations from individual mice suggest that ALK2 deficiency may influence how developing T cells progress through thymic stages, pointing to a possible role in guiding lineage outcomes. This could mean ALK2 plays a major role in stabilizing lineage outcomes during thymic maturation. Ongoing studies aim to determine whether ALK2 deficiency affects their persistence in peripheral compartments, or their phenotypic stability. Overall, this project aims to better understand how ALK2-dependent signaling influences immune tolerance by regulating T-cell development and Treg lineage integrity.
Faculty Advisor/Mentor
Piotr Kraj
Faculty Advisor/Mentor Email
pkraj@odu.edu
Faculty Advisor/Mentor Department
Biological Sciences
College/School Affiliation
College of Sciences
Student Level Group
Undergraduate
Presentation Type
Poster
Included in
Effects of ALK2 Deficiency on T Cell Fate and Regulatory T Cell Populations
Regulatory T cells (Tregs) are central to immune tolerance, and their lineage stability is established during thymic development and maintained in the periphery through tightly regulated signaling networks. Members of the BMP receptor family have been implicated in T-cell differentiation, yet the specific role of the type I receptor ALK2 in shaping cell fate and sustaining the regulatory program remains unclear. To examine how ALK2 contributes to T-cell development, we generated ALK2-knockout murine chimeras and analyzed lymphoid populations from the thymus, spleen, and peripheral tissues. Thymocytes and lymphocytes were isolated and stained with antibody panels to identify developmental subsets and regulatory populations. Samples were analyzed by flow cytometry to determine whether disruption of ALK2 signaling alters thymic selection, or CD4⁺ lineage commitment. Early observations from individual mice suggest that ALK2 deficiency may influence how developing T cells progress through thymic stages, pointing to a possible role in guiding lineage outcomes. This could mean ALK2 plays a major role in stabilizing lineage outcomes during thymic maturation. Ongoing studies aim to determine whether ALK2 deficiency affects their persistence in peripheral compartments, or their phenotypic stability. Overall, this project aims to better understand how ALK2-dependent signaling influences immune tolerance by regulating T-cell development and Treg lineage integrity.