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Production1
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Research Service, Department of Veteran Affairs Medical Center, and Division of Rheumatology and Clinical Immunology, University of Maryland School of Medicine, Baltimore, MD 21201;
Rheumatology Division, Veterans Affairs Medical Center and University of Cincinnati College of Medicine, Cincinnati, OH 45267; and
Specialized Center of Research in Systemic Lupus Erythematosus, Hospital for Special Surgery-Cornell University Medical Center, New York, NY 10021
The parent-into-F1 model of acute and chronic
graft-vs-host disease (GVHD) was used as an example of in vivo
cell-mediated or Ab-mediated responses, respectively, and the roles of
Fas and Fas ligand (FasL) were investigated. Using both flow cytometry
and PCR methodologies, we found that acute GVHD mice exhibited
significant up-regulation of Fas and FasL, whereas Fas/FasL
up-regulation in chronic GVHD mice was equal to or marginally greater
than that in uninjected mice. Functional studies confirmed that
Fas/FasL contributed to the anti-host CTL activity of splenocytes
from acute GVHD mice, although a perforin-dependent pathway was also
identified. Despite the presence of FasL on both donor CD4+
and CD8+ T cells in acute GVHD mice, depletion studies
demonstrated that all the in vitro anti-host CTL activity resided
in the CD8+ population. Furthermore, injection of
CD8-depleted B6 spleen cells into F1 mice blocked Fas/FasL
up-regulation and IFN-
production, resulting in chronic GVHD.
Lastly, up-regulation of Fas/FasL in acute GVHD mice could be blocked
by anti-IFN- mAb in vivo. Thus, in this in vivo model of
alloantigen immune responsiveness, Fas/FasL up-regulation is critically
dependent on Ag-specific (donor) CD8+ T cell activation and
IFN- production. Donor CD4+ T cell activation in the
absence of CD8+ T cell activation results in an
autoantibody-mediated response, no significant Fas/FasL up-regulation,
impaired elimination of autoreactive B cells, and persistent humoral
autoimmunity.
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