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Double mutant MRL‐ lpr/lpr‐gld/gld cells fail to trigger lpr ‐graft‐versus‐host disease in syngeneic wild‐type recipient mice, but can induce wild‐type B cells to make auto‐antibody
Author(s) -
Zhu Bangmin,
Beaudette Britte C.,
Rifkin Ian R.,
MarshakRothstein Ann
Publication year - 2000
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/1521-4141(200006)30:6<1778::aid-immu1778>3.0.co;2-d
Subject(s) - fas ligand , biology , effector , autoantibody , immunology , wild type , mutant , microbiology and biotechnology , antibody , apoptosis , genetics , programmed cell death , gene
Abstract Lethally irradiated mice reconstituted with histocompatible stem cells from Fas‐deficient MRL/lpr mice develop a wasting syndrome reminiscent of chronic graft‐versus‐host disease. However, reconstitution with double Fas‐/Fas ligand (FasL)‐deficient stem cells does not result in wasting disease, demonstrating that FasL expression is an important component of the effector mechanisms leading to this syndrome. In the absence of wasting disease double‐deficient T cells can induce wild‐type B cells to make autoantibodies. These data indicate that autoantibody production is regulated by FasL‐expressing T cells, and that Fas‐sufficient wild‐type B cells differ from Fas‐deficient lpr cells only with regard to their sensitivity to FasL.