T cells from mice with perinatal B7 blockade caused acute GVHD in syngeneic recipients. Pathogenicity of VSAg-reactive (a and b) and -nonreactive (c) T cells. (a) H&E staining of intestines (top) and lungs (bottom) from mice 4 wk after adoptive transfer of either 107 per mouse of bone marrow cells alone (left) or bone marrow plus 3 × 106 per mouse of VSAg-reactive T cells isolated from the thymi of mice perinatally treated with anti–B7-1 and anti–B7-2 mAbs (right). (b) Infiltration of Vβ3+ and Vβ11+ T cells in the intestine. Intestine sections, of mice that had received both bone marrow cells and VSAg-reactive T cells as described in panel a were stained with anti–Vβ3 (hamster) or anti–Vβ11 (rat) mAbs. Two sections of 40× and 200× are shown for each staining. Isotype controls (40×) for the two mAbs are shown in the top panels. (c) Mice that received thymocytes depleted of Vβ3, Vβ5, Vβ11, and Vβ12+ T cells developed severe inflammation of the lung (left), intestines (right), and liver (unpublished data). The details are as described in panel a, except that after depleting the VSAg-reactive T cells, the remaining CD4-enriched thymocytes (3 × 107 per mouse) and 107 syngeneic bone marrow cells were transferred into lethally irradiated syngeneic VSAg+ recipients.