The Role of Human Microbiota in Autoimmune Diseases: Exploring Dysbiosis and Mechanisms
Humans host between 10 and 100 trillion microbial cells, engaging in a mutually beneficial relationship with their microbiota. This intricate ecosystem supports both the microbes and their hosts, provided the body remains in good health. Estimates indicate that the human microbiota comprises over 1000 unique species of microorganisms, which play a crucial role in maintaining immune balance. They help modulate responses to harmless antigens and maintain the integrity of the intestinal mucosal barrier. When the gut microbiota becomes disrupted, a condition known as dysbiosis, it can lead to a range of immune disorders, including autoimmune diseases. Dysbiosis can influence the development and progression of inflammatory and autoimmune conditions by affecting immune system function and inflammatory responses. The present study aims to provide a comprehensive analysis of the relationship between microbiota and autoimmune diseases. It delves into how microbiota imbalances can contribute to autoimmune conditions and explores the underlying mechanisms involved. By integrating recent research and data, this study seeks to enhance our understanding of the microbiota's impact on autoimmune disease mechanisms and offer insights into potential therapeutic strategies.
Authors
- S. Naser Khaki
- Fatemeh Yazdanfar
- Ahmad Mobed (ORCID: https://orcid.org/0000-0001-8939-3688)
- Siavash Vadaye kheiri
- Sarvin Sanaie
- Hamed Abdollahi
- Shangyu Liu
Institutions
- Ahvaz Jundishapur University of Medical Sciences (IR)
- China Three Gorges University (CN)
- Tabriz University of Medical Sciences (IR)
- Islamic Azad University North Tehran Branch (IR)
- Islamic Azad University Medical Branch of Tehran (IR)
- Korea Health Promotion Institute (KR)
- Babol University of Medical Sciences (IR)
Publication Details
- Journal
- Apmis
- Published
- 2026-02-01
- DOI
- https://doi.org/10.1111/apm.70159
- Primary Topic
- Gut microbiota and health
- Type
- article
- Field-Weighted Citation Impact
- 0.00