Model
Digital Document
Publisher
Florida Atlantic University Digital Library
Description
T-lymphocytes develop from bone marrow derived hematopoietic stem cells (HSCs) and
mature in the thymus, where they participate in reciprocal signaling with thymic stromal
cells. The thymic developmental stages are well characterized, but only a few intrathymic
signals that influence the development of T-lymphocytes have been identified. Previous
microarray experiments revealed interleukin-17A (IL-17A) and its receptor (IL-17RA) as
a possible stromal-lymphoid signal. In this study, an IL-17RA-/- knockout was used to
determine whether the IL-17RA gene has a role in T-lymphocyte maturation. We made
competitive bone marrow chimeras and analyzed the percentage of donor wildtype and
mutant HSCs present in the bone marrow, and compared it to the percentage of a
particular blood cell type that developed from these donor HSCs. We found that IL-17RA
influences the maturation of T-lymphocytes, but does not affect the development of other
immune cells such as B-lymphocytes, macrophages, and granulocytes.
mature in the thymus, where they participate in reciprocal signaling with thymic stromal
cells. The thymic developmental stages are well characterized, but only a few intrathymic
signals that influence the development of T-lymphocytes have been identified. Previous
microarray experiments revealed interleukin-17A (IL-17A) and its receptor (IL-17RA) as
a possible stromal-lymphoid signal. In this study, an IL-17RA-/- knockout was used to
determine whether the IL-17RA gene has a role in T-lymphocyte maturation. We made
competitive bone marrow chimeras and analyzed the percentage of donor wildtype and
mutant HSCs present in the bone marrow, and compared it to the percentage of a
particular blood cell type that developed from these donor HSCs. We found that IL-17RA
influences the maturation of T-lymphocytes, but does not affect the development of other
immune cells such as B-lymphocytes, macrophages, and granulocytes.
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