Abstract

The effects of polyinosinic: polycytidylic acid (pl:C) on the graft-versus-host (GVH) reaction were studied. The drug pl:C rapidly and markedly induces interferon and augments natural killer (NK) cell activity. GVH reactions were induced by injecting parental lymphoid cells intravenously into F 1 hybrid mice. The development of a GVH reaction was monitored by measuring the plaque-forming cell (PFC) response to sheep red blood cells (SRBC) and by histological examination. When 30 × 10 6 B6 lymphoid cells were injected into B6AF 1 mice, the recipients developed profound immunosuppression by 10–12 days post-GVH induction. In addition, pathological changes indicative of GVH reactions were seen in the spleen, lymph nodes, thymus, liver, lung, pancreas, and salivary gland of these mice. However, the treatment of B6AF 1 recipients with pl:C prior to parental cell transfer markedly reduced the degree of suppression of the immune response, as measured by the PFC response to SRBC. Also, such mice failed to demonstrate the histological lesions of GVH disease. Treatment of donor mice with pl:C had no effect in preventing either GVH-induced immunosuppression or pathological changes. This study suggests that a pl:C-induced mechanism, possibly involving NK cells, is capable of regulating the GVH reaction.

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