GVHD reduces chemokine-driven OT-1 effector entry into extravascular BM but promotes PTX-sensitive OT-1 effector entry into GVHD target tissues. Irradiated CB6F1 mice were reconstituted with B6 BM with T cells (BM + T) or without B6 T cells (BM). On day +14 after transplantation, PTX-treated OT-1 effectors (Hoechst labeled) or untreated OT-1 cells (CMTMR labeled) were infused. Mice were euthanized 3 hours later, 3 minutes after being injected with an α-CD45.2 FITC antibody to identify intravascular cells. (A) Representative flow cytometry showing OT-1 cells from mice not injected with (top row) and injected with α-CD45.2 (second row). Representative CMTMR and Hoechst staining of CD8⁺vβ5⁺ cells is in the third row. Ratios of extravascular (CD45.2^–) to intravascular (CD45.2⁺) OT-1 cells (B). Enumeration of PTX⁺ and PTX^– OT-1 cells, paired from individual mice (C). Data are combined from 4 independent experiments with a total of 13 BM alone and 14 BM + T recipients. Too few OT-1 cells were recovered from some mice, especially in the colon, accounting for some groups having fewer than 13 or 14 data points. Significance was determined by a 2-tailed Student t test. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001. SP, spleen.