Autoimmune Hepatitis : Pathophysiology - 07/11/23

Doi : 10.1016/j.cld.2023.06.003

Zhou Yuming, MD ^a, Tang Ruqi, PhD ^a, Merrill Eric Gershwin, MD ^b,^⁎ , Ma Xiong, MD, PhD ^a,^c,^⁎
^a Division of Gastroenterology and Hepatology, Key Laboratory of Gastroenterology and Hepatology, Ministry of Health, NHC Key Laboratory of Digestive Diseases, State Key Laboratory for Oncogenes and Related Genes, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Institute of Digestive Disease, 145 Middle Shandong Road, Shanghai, China
^b Division of Rheumatology, Department of Medicine, Allergy and Clinical Immunology, University of California at Davis, 451 Health Sciences Drive, Suite 6510, Davis, CA 95616, USA
^c Institute of Aging & Tissue Regeneration, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

^∗Corresponding authors.

Résumé

Genome-wide association analyses suggest that HLA genes including HLA-DRB*0301, HLA-DRB*0401, and HLA-B*3501 as well as non-HLA genes including CD28/CTLA4/ICOS and SYNPR increased AIH susceptibility. The destruction of hepatocytes is the result of the imbalance between proinflammatory cells and immunosuppressive cells, especially the imbalance between Tregs and Th17 cells. The microbiome in patients with AIH is decreased in diversity with a specific decline in Bifidobacterium and enrichment in Veillonella and Faecalibacterium. Recent evidence has demonstrated the pathogenic role of E. gallinarum and L.reuteri in inducing autoimmunity in the liver.

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Keywords : Autoimmune hepatitis, Autoantibodies, T cells, Molecular mimicry, Immune regulation, Microbiome, Autoimmunity