@article {543061,
	title = {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.},
	journal = {J Immunol},
	volume = {157},
	number = {8},
	year = {1996},
	month = {1996 Oct 15},
	pages = {3250-9},
	abstract = {Efficient T cell proliferation requires costimulation via CD28/B7 or other pathways. Graft-vs-host disease (GVHD) is caused by activated donor T cells. We have found that the infusion of anti-B7.1 (CD80) + anti-B7.2 (CD86) mAb is effective in eliminating GVHD lethality induced by either CD8+ or CD4+ T cells. Donor CD4+ and CD8+ T cell expansion was inhibited by almost 100-fold as measured by enumerating thoracic duct lymphocytes (TDL) obtained early post-transplant. TDL retained anti-host responsiveness indicating that not all T cells were anergic. Although anti-CD80 or anti-CD86 mAb individually were ineffective in preventing CD8+ T cell GVHD lethality, each mAb was partially effective in CD4+ T cell-mediated GVHD. Because CD80 expression was found to be up-regulated on donor CD4+ TDL post-transplant, the GVHD capacity of donor CD4+ T cells deficient in CD80 was tested and found to be reduced similarly to that seen with anti-CD80 mAb. These studies demonstrate that anti-CD80 + anti-CD86 mAb infusion is effective in preventing GVHD lethality by inhibiting donor CD4+ or CD8+ T cell expansion and provide the first evidence that CD80 expression on donor T cells is critical for optimal GVHD lethality.},
	keywords = {Animals, Antibodies, Monoclonal, Antigens, CD, Antigens, CD80, Antigens, CD86, Bone Marrow Transplantation, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, Graft vs Host Disease, Histocompatibility Antigens Class II, Infusions, Intravenous, Membrane Glycoproteins, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Mice, SCID},
	issn = {0022-1767},
	author = {Blazar, B R and Sharpe, A. H. and Taylor, P A and Panoskaltsis-Mortari, A and Gray, G S and Korngold, R and Vallera, D A}
}
