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Effects of growth hormone and insulin‐like growth factor I binding to natural killer cells
Author(s) -
Bidlingmaier M.,
Auernhammer CJ,
Feldmeier H.,
Strasburger CJ
Publication year - 1997
Publication title -
acta paediatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.1997.tb18378.x
Subject(s) - endocrinology , medicine , natural killer cell , cd16 , growth factor , basal (medicine) , insulin like growth factor , major histocompatibility complex , interferon , immune system , biology , interleukin 21 , hormone , insulin , immunology , in vitro , t cell , cd3 , cytotoxic t cell , receptor , cd8 , biochemistry
Human growth hormone (GH) and insulin‐like growth factor I (IGF‐I) are known to bind to, and exert modulatory effects on, different immunocompetent cells, including CD16+/CD3– natural killer (NK) cells. NK cells are involved in various non‐major‐histocompatibility‐complex‐restricted actions of the immune system. Although no clinically significant defect in tumour or virus defence has been reported in GH‐deficient patients, the data available indicate decreased NK cell activity in these patients. In most studies, the absolute number and percentage of NK cells have been found to be normal. Substitution with GH has been reported to normalize the decreased NK cell activity in GH‐deficient patients. In a cross‐sectional study in GH‐deficient adults, decreased basal and interferon‐β (IFN‐β)‐stimulated NK cell activity was observed. In addition, IGF‐I was found to enhance basal and IFN‐β‐stimulated NK cell activity in vitro . Preliminary data on GH binding to NK cells indicate enhanced binding in GH‐deficient patients when compared with normal controls. □ Growth hormone deficiency, human growth hormone, insulin‐like growth factor I, natural killer cell activity