Symbiotic Regulatory Loop Between Foxp3+ T Cells, IgA and Gut Microbiota
Event details
| Date | 21.08.2013 |
| Hour | 12:15 › 13:15 |
| Speaker |
Prof. Sidonia Fagarasan, RIKEN, Yokohama (Japan) Bio: Sidonia Fagarasan completed training in clinical medicine at Iuliu Hatieganu University of Medicine and Pharmacy in 1990. She did residency and speciality in the Clinical Laboratory for Microbiology, Biochemistry and Hematology at the University of Medicine and Pharmacy, Cluj-Napoca, and was appointed to Assistant Professor in 1995. It was during this clinical period in Romania that Dr Fagarasan developed a fascination into the mechanisms governing intestinal immune homeostasis. In 1998, Dr Fagarasan was invited to Japan as a Mombusho Visiting Researcher and earned PhD from Kyoto University Faculty of Medicine in 2000. In Kyoto she contributed to the discovery of Activated Induced Deaminase (AID) with Tasuku Honjo and colleagues. She subsequently demonstrated the critical role of AID in gut homeostasis.Since 2002, Dr Fagarasan has been team leader of the Laboratory for Mucosal Immunity at the Research Centre for Allergy and Immunology (RCAI), RIKEN Yokohama, Japan. Dr. Fagarasan’s research primarily aims to elucidate mechanistic regulation and function of the mucosal antibody IgA in the gut. |
| Location | |
| Category | Conferences - Seminars |
A joint GLOBAL HEALTH & BIOENGINEERING Sandwich Seminar
The main function of the immune system is to protect the host against pathogens, such as bacteria or viruses. However, unlike the systemic immune system, the gut immune system does not eliminate microorganisms but instead nourishes rich bacterial communities and establishes advanced symbiotic relationships. Not only that the gut bacteria are essential for nutrient processing, production of vitamins and protection against pathogens (through competition for space and nutrients) but the development and maturation of the immune system depends on these bacteria.
The primary individual microbiota (Mb) probably reflect the maternal hand-over during or immediately after birth. However, the subsequent shaping of the microbial landscape is likely driven by complex interactions with the host immune system, through a network of regulatory components involving both the innate and adaptive immune system. Our previous studies demonstrated that the absence of immunoglobulin A (IgA) (the major effector molecule of the adaptive immunity in the gut), or the impaired IgA selection in germinal centers (GC) due to deregulated T cell control, severely affects the balance of gut bacterial communities, resulting in massive activation of the whole body immune system. The absence of a subset of regulatory CD4+ T cells induced by bacterial antigens to express Foxp3, also modifies the composition of gut Mb. Interestingly, the Foxp3+ T cells affect the IgA responses through their regulation of GC responses, and their depletion causes a rapid loss of specific IgA responses in the intestine. Together, all these observations point to the existence of a Foxp3-IgA axis in maintaining the balance of gut Mb and strongly suggest that the adaptive immune system may be a key mediator of host-bacterial symbiosis.
I will discuss our most recent findings of how the adaptive immune system is mediating host-microbial symbiosis, by controlling the diversification and balance of bacterial communities required for gut homeostasis and health.
The main function of the immune system is to protect the host against pathogens, such as bacteria or viruses. However, unlike the systemic immune system, the gut immune system does not eliminate microorganisms but instead nourishes rich bacterial communities and establishes advanced symbiotic relationships. Not only that the gut bacteria are essential for nutrient processing, production of vitamins and protection against pathogens (through competition for space and nutrients) but the development and maturation of the immune system depends on these bacteria.
The primary individual microbiota (Mb) probably reflect the maternal hand-over during or immediately after birth. However, the subsequent shaping of the microbial landscape is likely driven by complex interactions with the host immune system, through a network of regulatory components involving both the innate and adaptive immune system. Our previous studies demonstrated that the absence of immunoglobulin A (IgA) (the major effector molecule of the adaptive immunity in the gut), or the impaired IgA selection in germinal centers (GC) due to deregulated T cell control, severely affects the balance of gut bacterial communities, resulting in massive activation of the whole body immune system. The absence of a subset of regulatory CD4+ T cells induced by bacterial antigens to express Foxp3, also modifies the composition of gut Mb. Interestingly, the Foxp3+ T cells affect the IgA responses through their regulation of GC responses, and their depletion causes a rapid loss of specific IgA responses in the intestine. Together, all these observations point to the existence of a Foxp3-IgA axis in maintaining the balance of gut Mb and strongly suggest that the adaptive immune system may be a key mediator of host-bacterial symbiosis.
I will discuss our most recent findings of how the adaptive immune system is mediating host-microbial symbiosis, by controlling the diversification and balance of bacterial communities required for gut homeostasis and health.
Links
Practical information
- Informed public
- Free
- This event is internal
Organizer
- Prof. Nicola Harris