A Mechanism for the Suppression of Graft-vs-Host Disease with Endotoxin

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Abstract
It was shown that as few as 5 × 106 adherent spleen cells from CBA mice pretreated with endotoxin would suppress the GVH reactivity of 2 × 107 whole normal spleen cells from CBA mice when given to BALB/c neonates. This suppressive effect was also observed after the incubation of these two spleen cell populations in vitro for 2 hr. This adherent cell population of mice treated with endotoxin was characterized, and cell-cell contact was observed between macrophages and lymphocytes after in vitro incubation. Although no cell product was detected in the in vitro incubation environment, which impaired the GVH reactivity of 2 × 107 CBA whole normal spleen cells, as little as 0.1 ml of serum from endotoxin-treated mice, rich in IgM antibody, suppressed the GVH reactivity of 2 × 107 CBA whole normal spleen cells when given to BALB/c neonates. Endotoxin treatment of CBA mice also prevented normal rejection of allogenic skin and tumors. A mechanism is proposed in which adherent spleen cells and humoral factors from mice treated with endotoxin interact with normal spleen cells from CBA mice to abrogate the GVH disease in BALB/c neonates.