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SLE
Avemar induced a significant decrease in levels of all antibodies tested in mice with experimentally-induced SLE (systemic lupus erythematosus), an effect that was still detectable one month after the cessation of treatment with Avemar. This decrease in auto-antibody production is partly attributable to Avemar's influence on the Th1/Th2 cytokine system, in which it enhances Th1 activity (responsible for cellular immune response) and decreases Th2 activity (responsible for humoral immune response). An up-regulation of Th 1-related cytokines (IL-2, IFN?) and a down-regulation of Th 2 -related ones (IL-4, IL-10) were also demonstrated. It is important to note that, as the disease progresses, the activity of Th-2 system becomes more pronounced. The above results can be attributed to the immuno-modulatory effect of Avemar, supporting arguments for its clinical testing in SLE patients. Since an increase in cellular immune response is detectable even in this system, these findings do not contradict the immune-stimulating effect noted in cancer treatment.
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