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In Vitro Interleukin‐13 Production by Peripheral Blood in Patients with Newly Diagnosed Insulin‐Dependent Diabetes Mellitus and Their First Degree Relatives
Author(s) -
Kre ̧towski,
Myśliwiec,
Kinalska
Publication year - 2000
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.2000.00693.x
Subject(s) - first degree relatives , diabetes mellitus , insulin , medicine , autoantibody , endocrinology , proinflammatory cytokine , immunology , human leukocyte antigen , allele , antigen , biology , antibody , inflammation , family history , gene , genetics
It is generally accepted that proinflammatory cytokines secreted by macrophages/monocytes as well as cytotoxic T cells are responsible for pancreatic B‐cell destruction in animal models of autoimmune diabetes and presumably in insulin‐dependent diabetes mellitus (IDDM) in humans. The aim of the present study was to evaluate the production of interleukin (IL)‐13–a Th 2 cells derived anti‐inflammatory cytokine, by peripheral blood of newly diagnosed IDDM patients and their first degree relatives with a low or high risk of IDDM development. The study was carried out in 20 patients with a recent onset of type 1 diabetes, their first degree relatives with high (with DRB1*03 and/or DRB1*04 HLA class II alleles and two or more autoantibodies directed against pancreatic B‐cell antigens) ( n = 20) or a low (with DQB1*0602 allele) risk of type 1 diabetes development ( n = 10) and a control age matched group of healthy volunteers ( n = 18). IL‐13 concentrations in supernatant of 72 h cultures of peripheral blood after incubation with phytohemagglutinin (PHA) or PHA+ insulin were quantified by enzyme‐linked immunosorbent assay (ELISA). The levels of IL‐13 in the supernatants were significantly lower in at high risk of IDDM first degree relatives of diabetic patients ( P < 0.02), higher in subjects with low genetic risk of diabetes type 1 ( P < 0.02), and normal in IDDM patients in comparison to the control group. We have also observed that the adding of human insulin to the cultures resulted in a significant increase of in vitro IL‐13 production in prediabetics, but not in the other studied groups. In conclusion our findings suggest that the IL‐13 alterations could play an important role in the pathogenesis of type 1 diabetes. We would speculate that IL‐13 as an anti‐inflammatory cytokine and a mediator of the Th 2 pathway could be the potential therapeutic approach in the prevention of type 1 diabetes.