en ايمونولوژي Immunology پژوهشي Research <div style="text-align: justify;"><span style="font-size:11pt"><span style="background:white"><span sans-serif="" style="font-family:Calibri,"><strong><a name="_Hlk186053622"><u><span style="font-size:12.0pt"><span new="" roman="" style="font-family:" times=""><span style="color:#2f5496">Background & Objectives:</span></span></span></u></a></strong> <a name="_Hlk177670403"><span new="" roman="" style="font-family:" times="">This study explored the immunogenetic perspective underpinning the susceptibility and progression of ulcerative colitis (UC), a form of inflammatory bowel disease (IBD) characterized by chronic auto-inflammatory processes in the gut. This multifactorial disorder occurs in genetically predisposed individuals experiencing dysbiosis, wherein genetic factors contribute to intestinal imbalance and modulate immune pathways. Recent discoveries of novel genetic loci and polymorphisms have highlighted racial diversity in IBD susceptibility. Our research addresses a gap in the literature by examining the association between specific genetic loci and UC susceptibility in a defined ethnic group, aiming to identify and evaluate candidate genetic polymorphisms as part of an immunogenetic assessment to elucidate the mechanisms underlying UC susceptibility and progression.<span style="font-weight:normal"></span></span></a></span></span></span><br> <span style="font-size:11pt"><span style="background:white"><span sans-serif="" style="font-family:Calibri,"><strong><u><span style="font-size:12.0pt"><span new="" roman="" style="font-family:" times=""><span style="color:#2f5496">Materials & Methods:</span></span></span></u></strong> <span new="" roman="" style="font-family:" times="">In this case-control study, we evaluated 794 reference sequences (rs) from global, national, and regional ethnic databases, which were utilized for genotyping 150 control subjects via blood samples. We selected and investigated five genetic variants&mdash;rs3764147 (<i>LACC1</i> or <i>C13orf31</i>), rs763780 (<i>IL17F</i>), rs3749171 (<i>GPR35</i>), rs1260326 (<i>GCKR</i>), and rs4077515 (<i>CARD9</i>)&mdash;using Amplification-refractory mutation system polymerase chain reaction (ARMs PCR) followed by Sanger sequencing for confirmation in 50 UC patients.<span style="font-weight:normal"></span></span></span></span></span><br> <span style="font-size:11pt"><span style="background:white"><span sans-serif="" style="font-family:Calibri,"><strong><u><span style="font-size:12.0pt"><span new="" roman="" style="font-family:" times=""><span style="color:#2f5496">Results:</span></span></span></u> </strong><span new="" roman="" style="font-family:" times="">Analysis of the candidate genetic polymorphisms revealed that the <i>LACC1</i>, <i>IL17F</i>, and <i>GPR35</i> variants were significantly associated with UC, with the primary outcome focusing on this association and the secondary outcome examining the allelic frequencies of the five variants in both groups.<span style="font-weight:normal"></span></span></span></span></span><br> <span style="font-size:11pt"><span style="background:white"><span sans-serif="" style="font-family:Calibri,"><strong><u><span style="font-size:12.0pt"><span new="" roman="" style="font-family:" times=""><span style="color:#2f5496">Conclusion:</span></span></span></u></strong> <span new="" roman="" style="font-family:" times="">Ultimately, our findings demonstrate that the <i>GPR35</i> (G protein-coupled receptor 35) rs3749171, <i>IL17F</i> (Interleukin 17F) rs763780, and <i>LACC1</i> (laccase domain containing 1) rs3764147 variants contribute to UC susceptibility as a polygenic trait in the studied ethnic group. This underscores the potential importance of genetic architecture across different ethnicities, offering valuable biological insights into IBD pathogenesis and guiding future research.</span></span></span></span></div> Ulcerative colitis, LACC1, IL17F, GPR35, CARD9, Single Nucleotide Polymorphism (SNP) 77 101 http://jabs.fums.ac.ir/browse.php?a_code=A-10-490-9&slc_lang=en&sid=1 Mahsa Alem مهسا عالم mahsa.alem@gmail.com 100319475328460029526 100319475328460029526 No Department of Microbiology, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran گروه میکروبیولوژی، دانشکده دامپزشکی، دانشگاه ارومیه، ارومیه، ایران Seyyed Meysam Abtahi Froushani سید میثم ابطحی فروشانی meysamabtahi@hotmail.com 100319475328460029527 100319475328460029527 Yes Department of Microbiology, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran گروه میکروبیولوژی، دانشکده دامپزشکی، دانشگاه ارومیه، ارومیه، ایران Nasim Hajighahramani نسیم حاجی قهرمانی 100319475328460029528 100319475328460029528 No Department of Pharmaceutical Biotechnology, School of Pharmacy, Ardabil University of Medical Sciences, Ardabil, Iran گروه بیوتکنولوژی دارویی، دانشکده داروسازی، دانشگاه علوم پزشکی اردبیل، اردبیل، ایران Saied Hosseini-Asl سعید حسینی اصل 100319475328460029529 100319475328460029529 No Digestive Diseases Research Center, Ardabil University of Medical Sciences, Ardabil, Iran مرکز تحقیقات بیماری‌های گوارشی، دانشگاه علوم پزشکی اردبیل، اردبیل، ایران Farhad Pourfarzi فرهاد پورفرضی 100319475328460029530 100319475328460029530 No Digestive Diseases Research Center, Ardabil University of Medical Sciences, Ardabil, Iran مرکز تحقیقات بیماری‌های گوارشی، دانشگاه علوم پزشکی اردبیل، اردبیل، ایران Rasoul Nemati رسول نعمتی 100319475328460029531 100319475328460029531 No Department of Internal Medicine, Faculty of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran گروه داخلی، دانشکده پزشکی، دانشگاه علوم پزشکی اردبیل، اردبیل، ایران