Two patients with the Wiskott-Aldrichsyndrome had complete donor lymphoid and hematopoietic engraftment after successful allogeneic bone-marrow transplantation.
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The Wiskott-Aldrichsyndrome (WAS) is an X-linked recessive genetic disease in which the basic molecular defect is unknown.
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Background: Proliferation and IL-2 production in response to T-cell receptor ligation are impaired in patients with Wiskott-Aldrichsyndrome (WAS).
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This treatment of the Wiskott-Aldrichsyndrome may be a model for the correction of other genetically determined immune and hematologic bone-marrow disorders.
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The Wiskott-Aldrichsyndrome is an X-linked hereditary disorder associated with combined immunodeficiency, thrombocytopenia, small platelets, eczema, and increased susceptibility to autoimmune disorders and cancers.
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This mutation is likely to be the hypothesized genotype that caused the severe form of the Wiskott-Aldrichsyndrome in the three brothers described by Wiskott.
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Here we establish a fluorescence resonance energy transfer-based approach to visualize spatial and temporal regulation of neuronal Wiskott-Aldrichsyndrome protein (N-WASP) activity in living cells.
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The clinical data of 24 children with Wiskott-Aldrichsyndrome (WAS) from 23 unrelated Chinese families were reviewed in the present study.
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Earlier observations of defective CD43 expression by T lymphocytes from boys with the X-chromosome-linked Wiskott-Aldrichsyndrome suggested the importance of CD43 in lymphocyte function.
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A 28-year-old man with Wiskott-Aldrichsyndrome presented with ulcerative-proliferative lesions on his face from which herpes simplex type 1 (HSV-1) was isolated.