Onset of autoimmune lymphoproliferative syndrome (ALPS) in humans as a consequence of genetic defect accumulation-Reference-Cited by-同舟云学术

Onset of autoimmune lymphoproliferative syndrome (ALPS) in humans as a consequence of genetic defect accumulation

Published:2011-01-04 Issue:1 Volume:121 Page:106-112
ISSN:0021-9738
Container-title:Journal of Clinical Investigation
language:en
Short-container-title:J. Clin. Invest.

Author:

Magerus-Chatinet Aude,Neven Bénédicte,Stolzenberg Marie-Claude,Daussy Cécile,Arkwright Peter D.,Lanzarotti Nina,Schaffner Catherine,Cluet-Dennetiere Sophie,Haerynck Filomeen,Michel Gérard,Bole-Feysot Christine,Zarhrate Mohammed,Radford-Weiss Isabelle,Romana Serge P.,Picard Capucine,Fischer Alain,Rieux-Laucat Frédéric

Publisher

American Society for Clinical Investigation

Subject

General Medicine

Reference27 articles.

1. Chronic lymphadenopathy simulating malignant lymphoma

2. Increases in circulating and lymphoid tissue interleukin-10 in autoimmune lymphoproliferative syndrome are associated with disease expression

3. Dominant expression of interleukin 10 but not interferon γ in CD4- CD8- αβT cells of autoimmune lymphoproliferative syndrome

4. FAS-L, IL-10, and double-negative CD4−CD8− TCR α/β+ T cells are reliable markers of autoimmune lymphoproliferative syndrome (ALPS) associated with FAS loss of function

5. The development of lymphomas in families with autoimmune lymphoproliferative syndrome with germline Fas mutations and defective lymphocyte apoptosis

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