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- W2072367725 abstract "The molecular mechanisms that underlie T-cell quiescence are poorly understood. In the present study, we report a primary immunodeficiency phenotype associated with MST1 deficiency and primarily characterized by a progressive loss of naive T cells. The in vivo consequences include recurrent bacterial and viral infections and autoimmune manifestations. MST1-deficient T cells poorly expressed the transcription factor FOXO1, the IL-7 receptor, and BCL2. Conversely, FAS expression and the FAS-mediating apoptotic pathway were up-regulated. These abnormalities suggest that increased cell death of naive and proliferating T cells is the main mechanism underlying this novel immunodeficiency. Our results characterize a new mechanism in primary T-cell immunodeficiencies and highlight a role of the MST1/FOXO1 pathway in controlling the death of human naive T cells." @default.
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- W2072367725 date "2012-04-12" @default.
- W2072367725 modified "2023-10-16" @default.
- W2072367725 title "MST1 mutations in autosomal recessive primary immunodeficiency characterized by defective naive T-cell survival" @default.
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- W2072367725 doi "https://doi.org/10.1182/blood-2011-09-378364" @default.
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