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.
Primary Language | English |
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Subjects | Clinical Sciences |
Journal Section | Research Articles |
Authors | |
Publication Date | September 30, 2018 |
Published in Issue | Year 2018 Volume: 3 Issue: 3 |
Creative Commons Attribution Non-Commercial License: The articles in the Journal of Immunology and Clinical Microbiology are open access articles licensed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-sa/4.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.