In this study, we investigated whether an interleukin 2 (IL-2) secretion defect by peripheral blood mononuclear cells (PBMCs) after in vitro stimulation with phytohemagglutinin (PHA-M) occurs in either newly diagnosed or long-standing type I (insulin-dependent) diabetic patients and whether it is accompanied by a dysregulation of soluble IL-2— receptor (IL-2RS) production. PBMC cultures (2.5 × 106 cells), unstimulated or stimulated with PHA-M (25 μg/ml), from 20 type I diabetic patients (10 with time since onset <3 mo and 10 with long-term diabetes of <3 yr) and 10 control subjects were studied for the production of IL-2 and IL-2RS in their respective supernatants. No difference was found in IL-2 production in unstimulated cultures of type I patients compared with control subjects, although a significant decrease from PHA-M-stimulated cultures was seen (newly diagnosed, 1.7 ± 0.3 ng/2.5 × 106 cells; longstanding, 2.2 ± 0.3 ng/2.5 × 106 cells; P < .001 and P < .05, respectively) compared with control subjects (3.6 ± 0.4 ng/2.5 × 106 cells). In regard to the production of IL-2RS, no difference exists for unstimulated cultures, whereas, after PHA-M stimulation, both newly diagnosed and long-term-diabetic patients showed a decrease in the IL-2RS levels (318 ± 50 and 331 ± 62 U/2.5×106 cells; P < .02 and P < .05, respectively) compared with normal subjects (463 ± 34.2 U/2.5×106 cells). Thymus-activated cell phenotypes confirmed the T-lymphocyte activation after a 48-h culture period. The hypoproduction of IL-2 and IL-2RS in newly diagnosed patients may be the expression of the involvement of T-lymphocytes that have been activated continuously in vivo, but its presence in long-term patients suggests that the immunogenetic profile of the disease, involving immune-response genes also deputed to the control of lymphokine production levels, is such that type I diabetic patients are to be considered low IL-2 producers.
Original Articles|
March 01 1989
Interleukin 2 and Soluble Interleukin 2–Receptor Secretion Defect In Vitro in Newly Diagnosed Type I Diabetic Patients
Carla Giordano;
Carla Giordano
Laboratory of Immunology, Department of Clinica Medica, and Pa-tologia Generale, University of Palermo, School of Medicine
Palermo, Italy
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Felicia Pantò;
Felicia Pantò
Laboratory of Immunology, Department of Clinica Medica, and Pa-tologia Generale, University of Palermo, School of Medicine
Palermo, Italy
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Calogero Caruso;
Calogero Caruso
Laboratory of Immunology, Department of Clinica Medica, and Pa-tologia Generale, University of Palermo, School of Medicine
Palermo, Italy
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Maria A Modica;
Maria A Modica
Laboratory of Immunology, Department of Clinica Medica, and Pa-tologia Generale, University of Palermo, School of Medicine
Palermo, Italy
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Anna M Zambito;
Anna M Zambito
Laboratory of Immunology, Department of Clinica Medica, and Pa-tologia Generale, University of Palermo, School of Medicine
Palermo, Italy
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Nunzia Sapienza;
Nunzia Sapienza
Laboratory of Immunology, Department of Clinica Medica, and Pa-tologia Generale, University of Palermo, School of Medicine
Palermo, Italy
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Maria P Amato;
Maria P Amato
Laboratory of Immunology, Department of Clinica Medica, and Pa-tologia Generale, University of Palermo, School of Medicine
Palermo, Italy
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Aldo Galluzzo
Aldo Galluzzo
Laboratory of Immunology, Department of Clinica Medica, and Pa-tologia Generale, University of Palermo, School of Medicine
Palermo, Italy
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Address correspondence and reprint requests to Dr. C. Giordano, Laboratory of Immunology, Department of Clinica Medica, University of Palermo, Piazza delle Cliniche 2, 90127 Palermo, Italy.
Diabetes 1989;38(3):310–315
Article history
Received:
April 11 1988
Revision Received:
September 13 1988
Accepted:
September 13 1988
PubMed:
2783919
Citation
Carla Giordano, Felicia Pantò, Calogero Caruso, Maria A Modica, Anna M Zambito, Nunzia Sapienza, Maria P Amato, Aldo Galluzzo; Interleukin 2 and Soluble Interleukin 2–Receptor Secretion Defect In Vitro in Newly Diagnosed Type I Diabetic Patients. Diabetes 1 March 1989; 38 (3): 310–315. https://doi.org/10.2337/diab.38.3.310
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