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            <front>

                <journal-meta>
                                                                <journal-id>j immunol clin microbiol</journal-id>
            <journal-title-group>
                                                                                    <journal-title>Journal of Immunology and Clinical Microbiology</journal-title>
            </journal-title-group>
                                        <issn pub-type="epub">2528-9470</issn>
                                                                                            <publisher>
                    <publisher-name>Erkan YULA</publisher-name>
                </publisher>
                    </journal-meta>
                <article-meta>
                                        <article-id/>
                                                                <article-categories>
                                            <subj-group  xml:lang="en">
                                                            <subject>Clinical Sciences</subject>
                                                    </subj-group>
                                            <subj-group  xml:lang="tr">
                                                            <subject>Klinik Tıp Bilimleri</subject>
                                                    </subj-group>
                                    </article-categories>
                                                                                                                                                        <title-group>
                                                                                                                        <article-title>Distribution characteristics of RIG-I receptors of innate immunity in experimental diabetes mellitus and administration of nonspecific blockers of TNFα.</article-title>
                                                                                                                                        </title-group>
            
                                                    <contrib-group content-type="authors">
                                                                        <contrib contrib-type="author">
                                                                <name>
                                    <surname>Degen</surname>
                                    <given-names>Anna</given-names>
                                </name>
                                                            </contrib>
                                                                                </contrib-group>
                        
                                        <pub-date pub-type="pub" iso-8601-date="20180930">
                    <day>09</day>
                    <month>30</month>
                    <year>2018</year>
                </pub-date>
                                        <volume>3</volume>
                                        <issue>3</issue>
                                        <fpage>50</fpage>
                                        <lpage>59</lpage>
                        
                        <history>
                                    <date date-type="received" iso-8601-date="20180524">
                        <day>05</day>
                        <month>24</month>
                        <year>2018</year>
                    </date>
                                                    <date date-type="accepted" iso-8601-date="20180727">
                        <day>07</day>
                        <month>27</month>
                        <year>2018</year>
                    </date>
                            </history>
                                        <permissions>
                    <copyright-statement>Copyright © 2016, Journal of Immunology and Clinical Microbiology</copyright-statement>
                    <copyright-year>2016</copyright-year>
                    <copyright-holder>Journal of Immunology and Clinical Microbiology</copyright-holder>
                </permissions>
            
                                                                                                <abstract><p>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.</p></abstract>
                                                                                    
            
                                                            <kwd-group>
                                                    <kwd>type 1 diabetes mellitus</kwd>
                                                    <kwd>  RIG-like receptors</kwd>
                                                    <kwd>  retinoic acid-inducible gene-I</kwd>
                                            </kwd-group>
                                                        
                                                                                                                                                    </article-meta>
    </front>
    <back>
                            <ref-list>
                                    <ref id="ref1">
                        <label>1</label>
                        <mixed-citation publication-type="journal">1. Pino S, Kruger A, Bortell R. The role of innate immune pathways in type 1 diabetes pathogenesis. Curr Opin Endocrinol Diabetes Obes. 2010; 17 (2): 126–130.</mixed-citation>
                    </ref>
                                    <ref id="ref2">
                        <label>2</label>
                        <mixed-citation publication-type="journal">2.	Zhong Y, Kinio A, Saleh M. Functions of NOD-Like receptors in human diseases. Front Immunol. 2013; 16 (4): 333 338.</mixed-citation>
                    </ref>
                                    <ref id="ref3">
                        <label>3</label>
                        <mixed-citation publication-type="journal">3.	Yoneyama M, Fujita T. Structural mechanism of RNA recognition by the RIG-I-like receptors. Immunity 2008; 29: 178-185.</mixed-citation>
                    </ref>
                                    <ref id="ref4">
                        <label>4</label>
                        <mixed-citation publication-type="journal">4.	Kato H, Sato S, Yoneyama M. et al. Cell type-specific involvement of RIG-1 in antiviral response. Immunity. 2005; 23 (1): 19 28.</mixed-citation>
                    </ref>
                                    <ref id="ref5">
                        <label>5</label>
                        <mixed-citation publication-type="journal">5.	Yoneyama M, Kikuchi M, Matsumoto K, Imaizumi T, Miyagishi M, Taira K et al. Shared and unique functions of the DExD/H-box helicases RIG-I, MDA5, and LGP2 in antiviral innate immunity. J Immunol. 2005; 175: 2851 2858.</mixed-citation>
                    </ref>
                                    <ref id="ref6">
                        <label>6</label>
                        <mixed-citation publication-type="journal">6.	Kato H, Takeuchi O, Sato S. et al. Differential roles of MDA5 and RIG-I helicases in the recognition of RNA viruses. Nature. 2006, 441 (7089): 101 105.</mixed-citation>
                    </ref>
                                    <ref id="ref7">
                        <label>7</label>
                        <mixed-citation publication-type="journal">7.	Pichlmair A, Schulz O, Tan C.P., Naslund TI, Liljestrom P, Weber F, Reis C et al. RIG-I-mediated antiviral responses to single-stranded RNA bearing 5′-phosphates. Science. 2006; 314: 997–1001.</mixed-citation>
                    </ref>
                                    <ref id="ref8">
                        <label>8</label>
                        <mixed-citation publication-type="journal">8.	Alina Baum, Adolfo Garcı´a-Sastre Induction of type I interferon by RNA viruses: cellular receptors and their substrates. Amino Acids. 2010, 38: 1283–1299.9.	Kawai Т, Takahashi K, Sato S. et al. IPS-1, an adaptor triggering RIG-1 and Mda5-mediated type I interferon induction. Nat. Immunol. 2005; 6 (10): 981 988.</mixed-citation>
                    </ref>
                                    <ref id="ref9">
                        <label>9</label>
                        <mixed-citation publication-type="journal">10.	Takahashi K, Kawai Т, Kumar H. et al. Roles of caspase-8 and caspase-10 in innate immune responses to double-stranded RNA. J. Immunol. 2006; 176 (8): 4520 4524.</mixed-citation>
                    </ref>
                                    <ref id="ref10">
                        <label>10</label>
                        <mixed-citation publication-type="journal">11.	Takeuchi O, Akira S. Recognition of viruses by innate immunity. Immunol. Rev. 2007; 220: 214 224.</mixed-citation>
                    </ref>
                                    <ref id="ref11">
                        <label>11</label>
                        <mixed-citation publication-type="journal">12.	Heinig, M. et al. A trans-acting locus regulates an anti-viral expression network and type 1 diabetes risk. Nature. 2010; 467: 460–464.</mixed-citation>
                    </ref>
                                    <ref id="ref12">
                        <label>12</label>
                        <mixed-citation publication-type="journal">13.	Veckman V, Österlund P, Fagerlund R, Melén K, Matikainen S, Julkunen I. TNF-α and IFN-α enhance influenza-A-virus-induced chemokine gene expression in human A549 lung epithelial cells. Virology. 2006 Feb; 5: 96–104.</mixed-citation>
                    </ref>
                                    <ref id="ref13">
                        <label>13</label>
                        <mixed-citation publication-type="journal">14.	Ank N, West H, Bartholdy C, Eriksson K, Thomsen AR, Paludan SR. Lambda interferon (IFN-lambda), a type III IFN, is induced by viruses and IFNs and displays potent antiviral activity against select virus infections in vivo. J Virol. 2006 May; 80(9):4501 4509.</mixed-citation>
                    </ref>
                                    <ref id="ref14">
                        <label>14</label>
                        <mixed-citation publication-type="journal">15.	Poeck H, Bscheider M, Gross O et al. Recognition of RNA virus by RIG-I results in activation of CARD9 and inflammasome signaling for interleukin 1 beta production. Nat Immunol. 2010; 11: 63–69.</mixed-citation>
                    </ref>
                                    <ref id="ref15">
                        <label>15</label>
                        <mixed-citation publication-type="journal">16.	Kolumam GA., Thomas S, Thompson LJ, Sprent J, Murali-Krishna K. Type I interferons act directly on CD8 T cells to allow clonal expansion and memory formation in response to viral infection. J. Exp. Med.. 2005; 202: 637–650.</mixed-citation>
                    </ref>
                                    <ref id="ref16">
                        <label>16</label>
                        <mixed-citation publication-type="journal">17.	Curtsinger JM, Valenzuela JO, Agarwal P, Lins D, Mescher MF. Type I IFNs provide a third signal to CD8 T cells to stimulate clonal expansion and differentiation. J Immunol. 2005 Apr 15; 174(8):4465 4469.</mixed-citation>
                    </ref>
                                    <ref id="ref17">
                        <label>17</label>
                        <mixed-citation publication-type="journal">18.	Jego G, Palucka AK, Blanck JP, Chalouni C, Pascual V, Banchereau J. Plasmacytoid dendritic cells induce plasma cell differentiation through type I interferon and interleukin 6. Immunity. 2003; 19: 225–234.</mixed-citation>
                    </ref>
                                    <ref id="ref18">
                        <label>18</label>
                        <mixed-citation publication-type="journal">19.	Suthar MS, Ma DY, Thomas S, Lund JM, Zhang N, Daffis S, Rudensky AY, Bevan MJ, Clark EA, Kaja M-K et al. IPS-1 is essential for the control of West Nile virus infection and immunity. PLoS pathogens. 2010; 6(2):e1000757</mixed-citation>
                    </ref>
                                    <ref id="ref19">
                        <label>19</label>
                        <mixed-citation publication-type="journal">20.	Anz D, Koelzer VH, et al. Immunostimulatory RNA blocks suppression by regulatory T cells. J Immunol. 2010; 184(2): 939–946.</mixed-citation>
                    </ref>
                                    <ref id="ref20">
                        <label>20</label>
                        <mixed-citation publication-type="journal">21.	Hall JC, Rosen A. Type I interferons: crucial participants in disease amplification in autoimmunity. Nat Rev Rheumatol. 2010 Jan; 6(1): 40 49.</mixed-citation>
                    </ref>
                                    <ref id="ref21">
                        <label>21</label>
                        <mixed-citation publication-type="journal">22.	Qiao YF, Pang DZ, Lu JF, Hu BY, Liu D, Zhou GF, Yang B, Li RS, Jiang YS. Effect of potassium iodide on prevention of experimental lead nephropathy and expression of nuclear factor-kappaB and fibronectin. Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2009 Dec; 27(12):747 752.</mixed-citation>
                    </ref>
                                    <ref id="ref22">
                        <label>22</label>
                        <mixed-citation publication-type="journal">23.	Nejentsev S, Walker N, Riches D, Egholm M, Todd JA. Rare variants of IFIH1, a gene implicated in antiviral responses, protect against type 1 diabetes. Science. 2009 Apr 17; 324 (5925): 387 389.</mixed-citation>
                    </ref>
                                    <ref id="ref23">
                        <label>23</label>
                        <mixed-citation publication-type="journal">24.	Downes K, Pekalski M, Angus KL, Hardy M, Nutland S, Smyth DJ, Walker NM, Wallace C, Todd JA. Reduced expression of IFIH1 is protective for type 1 diabetes. PLoS One. 2010 Sep 9;5(9): 1264 1266.</mixed-citation>
                    </ref>
                            </ref-list>
                    </back>
    </article>
