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Original Article

Analysis of the Mechanism of Graft–Versus–Host–Like Disease in B6 Mice with Transferred B6-1Pr Spleen Cells

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Pages 307-315 | Received 27 Jun 1990, Published online: 07 Jul 2009
 

Abstract

Irradiated C57BL/6(B6) mice, when they were injected with spleen cells of C57BL/6J-Ipr/Ipr)(B6-lpr) mice, developed splenomegaly at 2 weeks post-transfer, but afterward displaced by GVH-like disease. At 2 weeks the enlarged spleen in the chimeric mice, designated as [B6-lpr → B6] chimera, contained about 70% of the total cell population as CD8-positive T cells.

Spleen cells from [B6-lpr → B6] chimeras were unresponsive to Con A and LPS stimulation and suppressed the mitogenic response of B6, B6-lpr, and C3H spleen cells to Con A. However, they had no cytotoxic activity towards Con A blasts of B6 and B6-lpr spleen cells. The suppressor activity found in the [B6–1 pr → B6] spleen cells was removed by pretreatment of them with anti-Thy-1.2 or anti-CD8(Lyt2.2) plus complement.

The present experiment showed that enormous proliferation of CD8-positive suppressor T cells was induced in the [B6-lpr → B6] chimeras. These cells were probably responsible for the GVH-like lymphoid atrophy observed in these [B6-lpr → B6] chimeras.

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