Distribution characteristics of RIG-I receptors of innate immunity in experimental diabetes mellitus and administration of nonspecific blockers of TNFα.
Öz
Background: We study type 1 diabetes as examples in which interactions between host and viruses have been implicated in autoimmune pathology. The RIG-I-like receptors (RLRs) as a sensors of RNA virus infection which can initiate and modulate antiviral immunity have been studied. The aim of the study was to determine the features of expression of retinoic acid-inducible gene-I (RIG-I) receptors in GALT in experimental diabetes mellitus (EDM) and after administration of pentoxifylline.
Materials and Methods: To determine structure of population of RIG +-cells we used the analysis of serial histological sections using the method of indirect immunofluorescense with monoclonal antibodies to RIG-I of rat (Santa Cruz Biotechnology, USA).
Results: It has been established that diabetes development was accompanied by an increase in total density RIG+ cells, population density of RIG+ macrophages and increase the concentration of the RIG protein in these cells in the lymphoid structures of ileum at 2nd week. But this data showed a dynamics to decrease to control values by the 4th week of disease. Pentoxifylline (PTX) administration of diabetic animals resulted in a decrease of the total density RIG+ cells, population density RIG+ dendritic cells and RIG+ lymphocytes on the at 2nd week of pathology, and on the 4th week of the disease this data showed dynamics to an increase.
Conclusions: All of these show that expression of RIG-I in ileum immunopositive cells can influence the differentiation of immunopositive cells and their ability to produce pro-inflammatory cytokines, thus acting as one of triggers of diabetes development and progression.
Anahtar Kelimeler
Kaynakça
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Ayrıntılar
Birincil Dil
İngilizce
Konular
Klinik Tıp Bilimleri
Bölüm
Araştırma Makalesi
Yazarlar
Anna Degen
Ukraine
Yayımlanma Tarihi
30 Eylül 2018
Gönderilme Tarihi
24 Mayıs 2018
Kabul Tarihi
27 Temmuz 2018
Yayımlandığı Sayı
Yıl 2018 Cilt: 3 Sayı: 3