dendritic cell stimulation by ifn-β alters t cell function via modulation of cytokine secretion in diabetes type 1

نویسندگان

saeid abediankenari department of microbiology and immunology, school of medicine, mazandaran university of medical sciences, sari, iran.

maryam ghasemi department of pathology, school of medicine, mazandaran university of medical sciences, sari, iran.

mohammad bagher eslami department of pathobiology, school of health, tehran university of medical sciences, tehran, iran.

چکیده

during antigen capture and processing, mature dendritic cells (dc) express large amounts of peptide-mhc complexes and accessory molecules on their surface. we investigated the role of ifn-β in induction hla-g expression on the monocyte derived dc and cytokine profile in diabetes type 1. we accomplished secretary pattern and total cytokine production of the th1 cytokine (il-2, γifn) and th2 cytokines (il-4, il-10) before and after mixed leukocyte reaction (mlr) of 30 diabetic patients and 30 normal subjects.     in this study a significant increase of il-10 and γifn reduction after ifn-β therapy in culture in presence of hla-g bearing dc as compared to control were seen. it is seen that dendritic cell causes il-10 production of t cell in vitro that reduce t cell activation from diabetes patients and normal subjects resulted to the production and expression of hla-g on these cells from both groups. using mixed leukocyte reaction, it was found that ifn-β-treated dendritic cell mediated the inhibition of autologous t cell activation via il-10 production and level of hla-g on dendritic cell may be correlated to disease activity in diabetes patients and it could also serve as a useful marker for disease progress and treatment.

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عنوان ژورنال:
acta medica iranica

جلد ۴۷، شماره ۵، صفحات ۳۴۱-۳۴۷

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