Not so Fas: Re-evaluating the mechanisms of immune privilege and tumor escape
- 1 May 2000
- journal article
- Published by Springer Nature in Nature Medicine
- Vol. 6 (5) , 493-495
- https://doi.org/10.1038/74955
Abstract
Based on early studies, it was hypothesized that expression of Fas ligand (FasL) by tumor cells enabled them to counterattack the immune system, and that transplant rejection could be prevented by expressing FasL on transplanted organs. More recent studies have indicated that the notion of FasL as a mediator of immune privilege needed to be reconsidered, and taught a valuable lesson about making broad conclusions based on small amounts of data.Keywords
This publication has 32 references indexed in Scilit:
- MATURE T LYMPHOCYTE APOPTOSIS—Immune Regulation in a Dynamic and Unpredictable Antigenic EnvironmentAnnual Review of Immunology, 1999
- Constitutive Expression of FasL in ThyrocytesScience, 1998
- Do CTL kill target cells by inducing apoptosis?Seminars in Immunology, 1997
- Contribution of Fas ligand to cardiac allograft rejectionInternational Immunology, 1996
- Prevention of Islet Allograft Rejection with Engineered Myoblasts Expressing FasL in MiceScience, 1996
- FLICE, A Novel FADD-Homologous ICE/CED-3–like Protease, Is Recruited to the CD95 (Fas/APO-1) Death-Inducing Signaling ComplexCell, 1996
- Fas Ligand-Induced Apoptosis as a Mechanism of Immune PrivilegeScience, 1995
- Ways around rejectionNature, 1995
- A role for CD95 ligand in preventing graft rejectionNature, 1995
- Viral inhibition of inflammation: Cowpox virus encodes an inhibitor of the interleukin-1β converting enzymeCell, 1992