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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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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 autoantibody.

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 Ipr cells only with regard to their sensitivity to FasL.[1]

References

  1. 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 autoantibody. Zhu, B., Beaudette, B.C., Rifkin, I.R., Marshak-Rothstein, A. Eur. J. Immunol. (2000) [Pubmed]
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