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Comment
. 2000 Sep;106(6):745-7.
doi: 10.1172/JCI11088.

Revisiting graft-versus-host disease models of autoimmunity: new insights in immune regulatory processes

W J Murphy  1
Affiliations
Comment

Revisiting graft-versus-host disease models of autoimmunity: new insights in immune regulatory processes

W J Murphy. J Clin Invest. 2000 Sep.
No abstract available

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Figures

Figure 1
Figure 1
Potential role for perforin (pfp) in immune homeostasis. Mutations in perforin have been shown to be responsible for CD8+ T-cell and macrophage hyperplasia, suggesting that immunoregulatory cells (possibly CD8+ T cells) use perforin for the suppression of these cells (blunt arrows). In a mouse model of GVHD, in which F1 hybrid animals receive lymphocytes from one of the parental strains (C57BL/6), donor CD4+ T cells promote host (shaded) B-cell expansion (pointed arrows). If unchecked, this expansion results in chronic GVHD. In this strain combination, donor CD8+ T cells mediate the elimination of the host B cells (blunt arrow) and result in acute GVHD. EBV has been shown to infect B cells and can result in the development of an EBV lymphoma. It is suggested here that CD8+ T cells might use the perforin-dependent pathway of target cell killing to suppress the proliferation of such EBV-infected B cells.
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References

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