Candida albicans in celiac disease: A wolf in sheep’s clothing |
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Institution: | 1. Department of Molecular Genetics, University of Toronto, Toronto, ON M5S 1A8, Canada;2. Lunenfeld-Tanenbaum Research Institute, Sinai Health System, Toronto, ON M5G 1X5, Canada;3. Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI 48109, USA;1. Gastroenterology and Hepatology Division, Joan and Sanford I. Weill Department of Medicine, Weill Cornell Medicine, New York, New York;2. The Jill Roberts Institute for Research in Inflammatory Bowel Disease, Weill Cornell Medicine, New York, New York;3. Department of Microbiology and Immunology, Weill Cornell Medicine, New York, New York;4. Immunology and Microbial Pathogenesis Program, Weill Cornell Graduate School of Medical Sciences, Weill Cornell Medicine, Cornell University, New York, New York;5. Kimmel Center for Biology and Medicine, Skirball Institute, New York University Grossman School of Medicine, New York, New York;6. Department of Microbiology, New York University Grossman School of Medicine, New York, New York;7. Division of Gastroenterology and Hepatology, Department of Medicine, New York University Langone Health, New York, New York;1. Department of Pediatrics, University of Texas, Southwestern Medical Center, Dallas, TX 75390, USA;2. Department of Pediatrics, Division of Hematology/Oncology, University of Texas, Southwestern Medical Center, Dallas, TX, USA;3. Department of Microbiology, University of Texas, Southwestern Medical Center, Dallas, TX, USA;4. Harold C. Simmons Cancer Center, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA |
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Abstract: | Candida albicans is a commensal fungus with a potential pathogenicity and celiac disease is an autoimmune condition. Both share multiple pathophysiological junctions, including serological markers against cell-wall proteins of Candida, anti-gliadin antibodies are positive in both entities, gluten and a candidal virulence factor share sequence similarity and the autoantigen of celiac disease, the tissue transglutaminase, is pivotal in Candida albicans commensalism and hostile behavior and its covalently cross linked products are stable and resistant to breakdown in the two entities. Those autoimmune/infectious cross roads are the basis for the hypothesis that Candida albicans is an additional environmental factor for celiac disease autoimmunogenesis. |
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