Briefly, we described 2 sisters in a family representing manifestations of Wiskott-Aldrich syndrome (WAS). The older sister had suffered from recurrent infections, small-sized thrombocytopenia, petechiase and purpura, and eczema for 7 years. The younger sister had the same manifestations, and died o
Intrinsic dendritic cell abnormalities in Wiskott-Aldrich syndrome
β Scribed by Michael Binks; Gareth E. Jones; Paul M. Brickell; Christine Kinnon; David R. Katz; Adrian J. Thrasher
- Publisher
- John Wiley and Sons
- Year
- 1998
- Tongue
- English
- Weight
- 150 KB
- Volume
- 28
- Category
- Article
- ISSN
- 0014-2980
No coin nor oath required. For personal study only.
π SIMILAR VOLUMES
Lymphocytes from patients with Wiskott-Aldrich syndrome (WAS) were studied 1) with prometaphase G banding to search for minor chromosome anomalies and 2) in mutagen stress assays to assess the extent of chromosome breakage under these conditions. One patient, a sporadic case of WAS, was found to hav
Wiskott-Aldrich syndrome (WAS), is an X-linked immunodeficiency disease caused by mutations of the WAS protein (WASP) gene, characterized by thrombocytopenia, eczema and recurrent infections. X-linked thrombocytopenia (XLT) is a milder form with only platelet abnormalities. Cumulative mutation data
Epstein-Barr virus (EBV) DNA was detected in immunoblastic lymphoma arising in a child with the primary immunodeficiency, Wiskott-Aldrich syndrome. Southern blot analysis of the structure of the EBV genome revealed that the lymphoma was monoclonal and contained episomal EBV DNA. The EBV latent genes