Hyperprolactinemia inhibits natural killer (NK) cell functionin vivo and its bromocriptine treatment not only corrects it but makes it more efficient

Springer Science and Business Media LLC - Tập 12 - Trang 210-215 - 1992
Antonio Vidaller1, Fernando Guadarrama1, Luis Llorente, Juan Pablo Méndez2, Fernando Larrea2, Antonio R. Villa1, Donato Alarcón-Segovia1
1Department of Immunology and Rheumatology, Instituto Nacional de la Nutrición Salvador Zubirán, México D.F., México
2Department of Reproductive Biology, Instituto Nacional de la Nutrición Salvador Zubirán, México D.F., México

Tóm tắt

We studied NK cell function in eight patients with pathological hyperprolactinemia by measuring51Cr release by K562 cells exposed to their mononuclear cells and found it decreased compared to normal controls (P<0.01). Bromocriptine (BrC) treatment corrected NK function but also made it more efficient at 12:1 than at 25:1 or 50:1 effector:target ratios (ANOVA;P=0.01). The study of NK cell function in agarose revealed that its decrease in hyperprolactinemia is due to their low active binding to target cells, active killing, and recycling capacity. BrC tended to correct them but also increased recycling capacity to levels higher than those of controls (P<0.05). Sequential studies in three hyperprolactinemic patients before and after BrC showed correction of NK function within 1 week but its increased efficiency at the 12:1 effector:target ratio required 8 weeks. We conclude that hyperprolactinemia decreases NK cell function. BrC corrects this by decreasing prolactin levels but also makes NK function more efficient by increasing the capacity of NK cells to recycle after killing.

Tài liệu tham khảo

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