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World J Gastroenterol. Oct 14, 2026; 32(38): 119677
Published online Oct 14, 2026. doi: 10.3748/wjg.119677
Published online Oct 14, 2026. doi: 10.3748/wjg.119677
Microbiota signatures and genetic risk in pediatric celiac disease
Ruveyda Akcin, Suat Saribas, Bekir Kocazeybek, Department of Medical Microbiology, Istanbul University-Cerrahpasa, Cerrahpasa Medical Faculty, İstanbul 34098, Türkiye
Ruveyda Akcin, Department of Medical Microbiology, Faculty of Medicine, Istanbul Health and Technology University, İstanbul 34320, Türkiye
Author contributions: Akcin R, Saribas S, and Kocazeybek B contributed to this paper; Kocazeybek B designed the overall concept; Akcin R contributed to the writing, discussion and design of the manuscript; Saribas S contributed to the editing the manuscript, illustrations, and review of literature. All authors have read and approved the final manuscript.
AI contribution statement: AI tools (Google Gemini) were used only for limited language assistance and editorial support, while the scientific content, interpretations, and intellectual framework of the manuscript were entirely developed by the authors.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Corresponding author: Bekir Kocazeybek, Professor, Department of Medical Microbiology, Istanbul University-Cerrahpasa, Cerrahpasa Medical Faculty, Kocamustafapaşa St No. 53, İstanbul 34098, Türkiye. bzeybek@istanbul.edu.tr
Received: February 3, 2026
Revised: April 22, 2026
Accepted: May 22, 2026
Published online: October 14, 2026
Processing time: 214 Days and 12.3 Hours
Revised: April 22, 2026
Accepted: May 22, 2026
Published online: October 14, 2026
Processing time: 214 Days and 12.3 Hours
Core Tip
Core Tip: Pediatric celiac disease cannot be explained by host genetics alone. Although human leukocyte antigen-DQ2 and human leukocyte antigen-DQ8 are necessary risk factors in most patients, they do not fully account for disease onset or clinical heterogeneity. Current evidence suggests that the gut microbiota, including bacterial, fungal, and viral communities, may act as a dynamic interface between genetic predisposition and environmental exposures. Longitudinal and functional studies in at-risk children may help define early microbial signatures and improve future risk stratification.