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Journal of Clinical Endocrinology & Metabolism, Vol 78, 635-641, Copyright © 1994 by Endocrine Society
ARTICLES |
H Kimata and A Yoshida
Department of Pediatrics, Kyoto University Hospital, Japan.
The effect of human GH and insulin-like growth factor-I (IGF-I) on immunoglobulin (Ig) production by and proliferation of human B cells was studied in serum- and hormone-free medium. GH enhanced the production of Ig by and thymidine uptake of the human lymphoblastoid B cell lines, CBL and GM-1056. IGF-I, but not IGF-II or insulin, also enhanced Ig production by and proliferation of CBL and GM-1056. However, the GH-induced enhancement was not mediated by IGF-I inasmuch as enhancement was blocked by anti-GH antibody but not by anti-IGF-I antibody or anti-IGF-I receptor antibody. Conversely, the IGF-I-induced enhancement was blocked by either anti-IGF-I antibody or anti-IGF-I receptor antibody but not by anti-GH antibody. GH and IGF-I also enhanced Ig production by and proliferation of the human lymphoblastoid B cell lines, CESS, GM-1500, SKW, and GM-3332. Furthermore, GH and IGF- I enhanced production of IgG1, IgG2, IgG3, IgG4, IgA1 IgA2, and IgM by and thymidine uptake of tonsillar B cells stimulated with Staphylococcus aureus Cowan strain I. Again, the GH-induced enhancement was blocked by anti-GH antibody whereas the IGF-I-induced enhancement was blocked by either anti-IGF-I antibody or anti-IGF-I receptor antibody but not vice versa.
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