Figure 1
Figure 1. Protection against GVHD after TLI/ATS conditioning is dependent on CD4+ T cells in the donor transplant. (A) Wild-type (WT) BALB/c host survival after 800 cGy TBI/ATS (n = 10) versus TLI/ATS (n = 8), followed by transplantation of 50 × 106 whole bone marrow cells and 60 × 106 splenocytes from wild-type C57BL/6 donors. Each group represents survival combined from 2 separate experiments. (B) Wild-type BALB/c host survival after TLI/ATS, followed by transplantation of 50 × 106 whole bone marrow and 60 × 106 splenocytes from CD4 T cell–deficient donors (CD4−/−; n = 10), CD8 T cell–deficient donors (CD8−/−; n = 10), invariant NKT cell–deficient donors (Jα18−/−; n = 8), or WT donors (n = 8). Each group represents survival combined from 2 to 3 separate experiments. (C) Mean body weight (± SE) at serial time points after transplantation in wild-type BALB/c hosts receiving either 800 cGy TBI/ATS or TLI/ATS and 50 × 106 whole bone marrow and 60 × 106 splenocytes from wild-type donors, or wild-type TLI/ATS-conditioned hosts given CD4−/− donor bone marrow and splenocyte transplants. + indicates analysis was stopped when 2 hosts remained in the group. (D) Mean (± SE) histopathologic GVHD scores of colon, skin, and liver at day 6 from 3 groups of hosts from panel C. n = 5-8 for all groups. (E) Microscopic examination of hematoxylin/eosin-stained sections of colon at day 6 in 1 representative host from each group shown in panels C and D. WT BALB/c host given TBI/ATS with WT donor cells shows evidence of inflammatory infiltrate (*) and loss of normal crypt architecture in the colon, with separation of crypts by inflammation, lifting off of crypts from the basement membrane, and multiple areas of apoptotic crypt nuclei (→). WT BALB/c host given TLI/ATS conditioning with WT donor cells shows normal appearance. WT host given TLI/ATS and CD4−/− donor cells shows inflammatory infiltrate (*) and loss of normal crypt architecture in the host colon, with separation of crypts by inflammation and lifting off of crypts from the basement membrane. Specimens shown are at 300× final magnification.

Protection against GVHD after TLI/ATS conditioning is dependent on CD4+ T cells in the donor transplant. (A) Wild-type (WT) BALB/c host survival after 800 cGy TBI/ATS (n = 10) versus TLI/ATS (n = 8), followed by transplantation of 50 × 106 whole bone marrow cells and 60 × 106 splenocytes from wild-type C57BL/6 donors. Each group represents survival combined from 2 separate experiments. (B) Wild-type BALB/c host survival after TLI/ATS, followed by transplantation of 50 × 106 whole bone marrow and 60 × 106 splenocytes from CD4 T cell–deficient donors (CD4−/−; n = 10), CD8 T cell–deficient donors (CD8−/−; n = 10), invariant NKT cell–deficient donors (Jα18−/−; n = 8), or WT donors (n = 8). Each group represents survival combined from 2 to 3 separate experiments. (C) Mean body weight (± SE) at serial time points after transplantation in wild-type BALB/c hosts receiving either 800 cGy TBI/ATS or TLI/ATS and 50 × 106 whole bone marrow and 60 × 106 splenocytes from wild-type donors, or wild-type TLI/ATS-conditioned hosts given CD4−/− donor bone marrow and splenocyte transplants. + indicates analysis was stopped when 2 hosts remained in the group. (D) Mean (± SE) histopathologic GVHD scores of colon, skin, and liver at day 6 from 3 groups of hosts from panel C. n = 5-8 for all groups. (E) Microscopic examination of hematoxylin/eosin-stained sections of colon at day 6 in 1 representative host from each group shown in panels C and D. WT BALB/c host given TBI/ATS with WT donor cells shows evidence of inflammatory infiltrate (*) and loss of normal crypt architecture in the colon, with separation of crypts by inflammation, lifting off of crypts from the basement membrane, and multiple areas of apoptotic crypt nuclei (→). WT BALB/c host given TLI/ATS conditioning with WT donor cells shows normal appearance. WT host given TLI/ATS and CD4−/− donor cells shows inflammatory infiltrate (*) and loss of normal crypt architecture in the host colon, with separation of crypts by inflammation and lifting off of crypts from the basement membrane. Specimens shown are at 300× final magnification.

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