Infusion of anti-B7.1 (CD80) and anti-B7.2 (CD86) monoclonal antibodies inhibits murine graft-versus-host disease lethality in part via direct effects on CD4+ and CD8+ T cells.

摘要: Efficient T cell proliferation requires costimulation via CD28/B7 or other pathways. Graft-vs-host disease (GVHD) is caused by activated donor cells. We have found that the infusion of anti-B7.1 (CD80) + anti-B7.2 (CD86) mAb effective in eliminating GVHD lethality induced either CD8+ CD4+ Donor and expansion was inhibited almost 100-fold as measured enumerating thoracic duct lymphocytes (TDL) obtained early post-transplant. TDL retained anti-host responsiveness indicating not all cells were anergic. Although anti-CD80 anti-CD86 individually ineffective preventing lethality, each partially cell-mediated GVHD. Because CD80 expression to be up-regulated on post-transplant, capacity deficient tested reduced similarly seen with mAb. These studies demonstrate inhibiting provide first evidence critical for optimal lethality.