Transfer factor therapy in multiple sclerosis: a three-year prospective double-blind clinical trial.

One hundred five patients with MS were divided into three groups matched for age, sex, and disability, and treated with either placebo, transfer factor prepared from leukocytes of random donors, or transfer factor from leukocytes of family members living with the patients. There were no differences in the three treatment groups for changes in disability, activities of daily living, or evoked potentials. Eighteen months of transfer factor therapy had no effect on gamma-interferon production or natural killer cell activities.

In vitro correction of the interleukin-2 and interferon-gamma defect in multiple sclerosis.

The effect of phytohaemagglutinin (PHA) and/or phorbol myristic acetate (PMA) on human interferon-gamma (HuIFN-gamma) and interleukin 2 (IL-2) production was measured in peripheral blood leucocytes (PBL) from multiple sclerosis (MS) patients. Seven out of 12 MS patients studied had PBLs which were unable to produce any detectable HuIFN-gamma after stimulation with PHA. The PBL cultures of the same seven patients were also defective for IL-2 production after PHA stimulation.

Influence of prostaglandin E2 and indomethacin on interferon-gamma production by cultured peripheral blood leukocytes of multiple sclerosis patients and healthy donors.

The addition of indomethacin to concanavalin A (Con A)-induced cultures of human peripheral blood leukocytes (PBL) caused an increase in interferon response, regardless of whether the PBLs were derived from multiple sclerosis (MS) patients or from control donors. Specifically the response rates increased from 71 to 100% in controls and from 24 to 53% in MS patient-derived cultures. The amounts of interferon produced also increased in both groups by 0.

Interferon-gamma production by peripheral blood leucocytes from patients with multiple sclerosis and other neurological diseases.

Peripheral blood leucocyte (PBL) cultures of patients with meningoencephalitis, myasthenia gravis, Alzheimer's dementia, Huntington's chorea as well as patients who were recovering from cerebrovascular accidents or from craniotomy for brain tumours, all had defective interferon-gamma (IFN-gamma) responses to stimulation with concanavalin A (Con A) and phytohaemagglutinin (PHA), similar to those already described for PBL cultures of patients with multiple sclerosis. Specifically, cultures from a significant percentage of the patients failed to produce IFN after stimulation with either of the two mitogens. The yields from those cultures that did respond were not significantly lower than those from cultures of healthy blood donors.