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

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, demo...

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Veröffentlicht in:	European journal of immunology 2000-06, Vol.30 (6), p.1778-1784
Hauptverfasser:	Zhu, Bangmin, Beaudette, Britte C., Rifkin, Ian R., Marshak‐Rothstein, Ann
Format:	Artikel
Sprache:	eng
Schlagworte:	Anti‐nuclear antibody Fas antigen Fas ligand FasL protein Graft‐versus‐host disease Inflammation Radiation chimera
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creator	Zhu, Bangmin Beaudette, Britte C. Rifkin, Ian R. Marshak‐Rothstein, Ann
description	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.
doi_str_mv	10.1002/1521-4141(200006)30:6<1778::AID-IMMU1778>3.0.CO;2-D
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source	Wiley Online Library Journals Frontfile Complete; Wiley Online Library Free Content; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals
subjects	Anti‐nuclear antibody Fas antigen Fas ligand FasL protein Graft‐versus‐host disease Inflammation Radiation chimera
title	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
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