SUMMARYThe continuous infusion of the opioid peptide b-endorphin prolongs skin allograft survival in mice, while the opiate receptor antagonist naloxone, administered together with the opioid at the time of transplantation, abolishes the effect of the opioid. Consistently, naloxone, when given alone at the time of transplantation, but not later, accelerates graft rejection and increases splenocyte IL-2 and interferongamma (IFN-g) production. Splenocyte b-endorphin concentrations are lower in transplanted animals. The effects of exogenous b-endorphin and naloxone suggest that the endogenous opioid peptide bendorphin exerts a tonic inhibitory effect over early events of T cell-mediated immune responses in vivo. The effects of b-endorphin and naloxone are consistent with the previously shown role of the opioid system in the modulation of the Th1/Th2 cytokine pattern.

The red cell-monocyte assay (RMA), which has been used to evaluate the clinical significance of red cell (RBC) antibodies, was employed to test the effect of the dialyzable leukocyte extract (DLE) on in vitro adherence to monocytes of human RBCs coated with alloantibodies or autoantibodies. The total association index (TAI) of the RMA, expressing the number of RBCs adhering to or phagocytosed by 100 monocytes, indicated a potent inhibitory activity of DLE in the test system. TAI values of 100.4 +/- 20.1 (mean +/- SD) in the control sample, consisting of RBCs coated in vitro with anti-D, dropped to 4.0 +/- 2.1 when DLE was present in the assay medium at a concentration of 0.5 U per mL. Similar results were obtained with RBCs coated with IgG antibodies in vivo. The inhibition was dose dependent and was associated with a thermolabile component of DLE. This study establishes that DLE can modulate monocyte function by inhibiting the recognition of IgG sensitized red cells.

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