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* Instituto de Investigaciones Bioquímicas Fundación Campomar (IIB-UBA and IIBBA CONICET),
Instituto de Biología y Medicina Experimental CONICET, and
Laboratorio de Patología Sanatorio Mater Dei, Buenos Aires, Argentina
Correspondence: Alicia Roldán, Instituto de Biología y Medicina Experimental, Vuelta de Obligado 2490, 1428 Buenos Aires, Argentina. E-mail: aroldan{at}dna.uba.ar
This study evaluates the effects of insulin-like growth factor (IGF)-1 receptor (IGF-1R) down-regulation in stimulated T lymphocytes by investigating the expression of early activation proteins CD69, CD25, and interleukin (IL)-2. We found that IGF-1 does not modify CD69 expression but increases transcription and protein synthesis of CD25 and IL-2. The lowest level of IGF-1R detected after 15 min of activation suggested that the effects of IGF-1 occur at the initiation of cell activation. The activation of IGF-1R was confirmed by IGF-1R phosphorylation and increased phosphorylation of microtubule-associated protein kinase. We also detected the alternative IGF-1 transcripts Ea, with paracrine/autocrine regulation, and Eb, with endocrine regulation, in Jurkat cells and in quiescent T lymphocytes, and we detected IGF-1 protein in the culture medium after stimulation. These data suggest that the proliferative effects of IGF-1 on T lymphocytes include both autocrine/paracrine and endocrine processes.
Key Words: CD25 IL-2 IGF-1 receptor IGF-1 mRNA MAPK
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