Abstract
ABSTRACT: We used an in vitroT-lymphoblast clonal proliferation assay to quantify human IGF-I (hIGF-I)-, human PTH (hPTH)-, human ACTH (hACTH)-, and human TSH (hTSH)-stimulated growth of human T-cell leukemia virus-II-transformed T-lymphoblast cell lines from normal individuals and to elucidate the role of IGF-I as the mediator of hPTH-, hACTH-, and hTSH-induced T-cell growth. Normal T-lymphoblast cell lines respond to hIGF-I in a bimodal fashion. The mean first peak response was 143 ± 9.8% above baseline (defined as 100%) occurring at 8 μg/L, and the mean second peak response was 154 ± 14.4% occurring at 100 μ/L. Both responses were completely blocked after incubation with αIR-3, an MAb to the IGF-I receptor (by analysis of variance, p= 0.015 between full response curves). After stimulation with hPTH, the mean peak clonal response of normal T-lymphoblast cell lines was 189 ± 7.0%; after incubation with αIR-3, the mean peak clonal response was 108 ± 7.9% (p= 0.0015 between full response curves). The mean peak clonal response of normal T-lymphoblast cell lines after hACTH stimulation was 192 ± 8.6%; preincubation with αIR-3 reduced the mean peak clonal response to 94 ± 1.2% (p< 0.0001 between full response curves). With hTSH stimulation, the mean peak clonal response of normal T-lymphoblast cell lines was 167 ± 7.0%; after incubation with αR-3, the mean peak clonal response was 94 ± 8.2% (p= 0.003 between full response curves). After stimulation with hIGF-I, hPTH, hACTH, and hTSH, the mean peak clonal responses of a pygmy T-lymphoblast cell line were 112 ± 8.2, 122 ± 1.5. 99 ± 4.2. and 98 ± 5.5%, respectively (all p≤ 0.0004 between corresponding complete pygmy and normal response curves). These data indicate that hPTH, hACTH, and hTSH stimulate growth of normal human T-lymphoblast cell lines through local action of IGF-I, because these effects can all be blocked by preincubation with MAb against the IGF-I receptor. The pygmy T-lymphoblast cell line showed little or no clonal expansion in the presence of hIGF-1 itself, or in response to hPTH, hACTH, or hTSH, further supporting the notion that an intact IGF-I response mechanism is necessary for the proliferative response to hPTH, hACTH, and hTSH in human T-lymphoblasts.
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Geffner, M., Bersch, N., Cortez, A. et al. Growth-Promoting Actions of Parathyroid Hormone, Adrenocorticotrophic Hormone, and Thyroid-Stimulating Hormone: In Vitro Studies in Normal and Pygmy T-Lymphoblast Cell Lines. Pediatr Res 37, 507–511 (1995). https://doi.org/10.1203/00006450-199504000-00021
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DOI: https://doi.org/10.1203/00006450-199504000-00021