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- W4313384955 abstract "Abstract Bone marrow failure occurs when the bone marrow cannot produce sufficient numbers of red blood cells, white blood cells or platelets. Bone marrow failure disorders are rare, yet serious conditions, and are often thought to be the result of immune destruction within the bone marrow. IL-2-deficient mice, which have a deficit in functional regulatory T cells, develop spontaneous bone marrow failure. We show that disease occurs in these mice with a specific accumulation of T cells in the bone marrow, a shift in the CD4/CD8 ratio, IFNγ-mediated hematopoietic stem cell dysfunction, and antibodies directed against bone marrow and bone tissue, recapitulating human disease, and suggesting that this disease may be caused by self-reactive immune responses. Disease onset is rapid at 12 days of age with death by 27 days, and T cell responses are essential for disease progression, providing a novel model for defining the immune cell dysregulation in this autoimmune disease. We use this model to define the mechanisms underlying the deficit in myelopoiesis observed during bone marrow failure, including the contribution of activated lymphocyte subsets to disease induction. Our study describes the influence of IFNγ, CD4 and CD8 T cell subsets, and local bone marrow proliferation and migration on the kinetics and severity of disease." @default.
- W4313384955 created "2023-01-06" @default.
- W4313384955 creator A5023561897 @default.
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- W4313384955 date "2017-05-01" @default.
- W4313384955 modified "2023-09-27" @default.
- W4313384955 title "T cell mediated mechanisms underlying HSC dysfunction and bone marrow failure" @default.
- W4313384955 doi "https://doi.org/10.4049/jimmunol.198.supp.207.21" @default.
- W4313384955 hasPublicationYear "2017" @default.
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