Nontoxic concentrations of retinoic acid enhance DNA synthesis of human peripheral blood lymphocytes in response to phytohemagglutinin or rabbit-antihuman-thymocyte globulin, whereas the response to concanavalin A or pokeweed mitogen remained unaffected. Retinoic acid-induced stimulation of lymphocyte reactivity to phytohemagglutinin or antithymocyte globulin was most evident in T cell-enriched subpopulations and required the near-concurrent addition of retinoic acid and mitogens. Retinoic acid-mediated enhancement of lymphocyte proliferation in response to phytohemagglutinin or antithymocyte globulin was paralleled by a concomitant suppression of immune interferon production of lymphocytes stimulated with these mitogens. These findings allow further studies on the immunoregulatory action of retinoids in vitro.

Non-toxic concentrations of retinoic acid (RA) inhibited the spontaneous activity of human natural killer (NK) cells. RA also inhibited the activation of human NK cells by treatment with partially purified human leukocyte interferon (HulFN alpha) or with inducers of IFN alpha and IFN gamma. Full expression of the inhibitory action required prolonged exposure of human peripheral blood leukocytes to RA. Implications of these findings for the use of retinoids in the treatment of human malignancies are discussed.

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Peripheral blood leukocytes from patients with chronic hepatitis B virus (HBV) infection were studied for their capacity to produce interferon (IFN) alpha or IFN gamma. Yields of IFN alpha in leukocyte cultures stimulated with influenza A virus or human leukemic cells were significantly lower than those obtained from healthy controls. Production of IFN gamma in response to induction with protein A of Staphylococcus aureus was also significantly diminished. Defects of IFN production in leukocyte cultures showed no correlation with active viral replication or the degree of severity of HBV-associated liver disease. The demonstration of partial defects of endogenous IFN production provides a rationale for using IFN replacement therapy in patients with chronic HBV infection.