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Biomedical subjects

B Kotsy

Publications and source records attributed to B Kotsy.

2 recordsLinked to original sources

Lack of correlation between impaired interferon production and natural killer activity of lymphocytes in multiple sclerosis.

The ability of lymphocytes from patients with multiple sclerosis (MS) to produce Interferon (IFN-alpha) in response to Newcastle Disease Virus (NDV) was studied in vitro. The correlation between individual IFN-alpha titers and natural killer (NK) cell activity and the presence of HLA system antigens associated with MS (B-7 and DRW-2) was also investigated. Lymphocytes from MS patients showed a significantly impaired capacity to synthesize IFN-alpha in vitro when compared to lymphocytes from healthy donors (mean titers: 85.9 I.U. and 268.2 I.U., respectively). Marked differences in IFN-alpha titers were observed in the group of MS patients. The production of IFN-alpha by the patients' lymphocytes did not correlate with either the activity of NK cells or with their stimulation by exogenous IFN-alpha. There was also no correlation between IFN-alpha production by lymphocytes from MS patients and the presence or absence of B-7 and DRW-2 antigens.

Adolescent↗

Dysfunction of natural killer cells in multiple sclerosis: a possible pathogenetic factor.

Natural killer (NK) cell activity, antibody-dependent cytotoxicity (ADCC) and the effect of interferon on NK activity was investigated in multiple sclerosis (MS) patients. NK activity measured against K-562 tumour cell line was found to be significantly low in MS patients, and this was most pronounced in the group of male patients with definitive disease. The response of NK cells to interferon proved to be impaired and almost no activation could be demonstrated in response to polyinosinic-polycytidylic acid (poly I:C). Preliminary data obtained by the determination of interferon production in several definitive MS cases reflect a defect in the interferon producing capacity of lymphocytes. The possible involvement of impaired NK cell function in the aetiopathogenesis of MS is discussed.

Adult↗