Figure 7.
Figure 7. 3H3 treatment reverses advanced cGVHD. (A-B) At 6 weeks after disease induction, cGVHD mice were administered 200 μg 3H3 alone () or infusion of 8 × 107 DBA/2 spleen/lymph node cells (▪) (A). In panel B, one group of cGVHD mice was administered control Ig (), and the other, 3H3 (▴). Autoantibody production was measured from 1 to 2 weeks thereafter. OD values are shown as means ± SD of 10-fold dilution of samples of n = 4-5 per group. *P < .05 between the 2 groups at the indicated times. (C) Control Ig or 3H3 was injected into cGVHD mice 2 weeks after disease induction. Splenocytes were harvested 7 days after antibody treatment, and donor CD4+ T cells and B cells were counted by staining with anti–H-2Kb plus anti-CD4 or anti-B220, respectively. Autoreactive B cells producing anti-DNA IgG1 were counted using ELISPOT. *P < .05 between the 2 groups.

3H3 treatment reverses advanced cGVHD. (A-B) At 6 weeks after disease induction, cGVHD mice were administered 200 μg 3H3 alone () or infusion of 8 × 107 DBA/2 spleen/lymph node cells (▪) (A). In panel B, one group of cGVHD mice was administered control Ig (), and the other, 3H3 (▴). Autoantibody production was measured from 1 to 2 weeks thereafter. OD values are shown as means ± SD of 10-fold dilution of samples of n = 4-5 per group. *P < .05 between the 2 groups at the indicated times. (C) Control Ig or 3H3 was injected into cGVHD mice 2 weeks after disease induction. Splenocytes were harvested 7 days after antibody treatment, and donor CD4+ T cells and B cells were counted by staining with anti–H-2Kb plus anti-CD4 or anti-B220, respectively. Autoreactive B cells producing anti-DNA IgG1 were counted using ELISPOT. *P < .05 between the 2 groups.

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