CD101 as an indicator molecule for pathological changes at the interface of host-microbiota interactions
Marius Wrage1, Johanna Kaltwasser1, Sonja Menge1
1Mikrobiologisches Institut - Klinische Mikrobiologie, Immunologie und Hygiene, Universitätsklinikum Erlangen and Friedrich-Alexander Universität (FAU) Erlangen-Nürnberg, Erlangen, Germany.
International Journal of Medical Microbiology : IJMM
|March 27, 2021
Summary
Intestinal microbiota influence immune responses and are linked to inflammatory bowel disease (IBD) and type 1 diabetes (T1D). Reduced CD101 expression on immune cells in these conditions may stem from gut dysbiosis and inflammation.
Area of Science:
- Immunology
- Microbiology
- Gastroenterology
Background:
- Intestinal microbiota regulate host biochemical, metabolic, and immunological processes.
- Disruptions in host-microbiota interactions contribute to immune-mediated disorders like IBD and T1D.
- Altered gut microbiota and increased intestinal permeability are hallmarks of IBD and T1D.
Purpose of the Study:
- To investigate the role of CD101 expression on immune cells in the context of IBD and T1D.
- To explore the relationship between intestinal microbiota composition and CD101 expression.
- To understand how dysbiosis impacts immune cell function in these diseases.
Main Methods:
- Analysis of CD101 expression on myeloid cells, intraepithelial lymphocytes (IELs), and regulatory T cells (Tregs).
- Assessment of immune cell profiles and cytokine production.
- Correlation of CD101 expression with intestinal microbiota composition and bacterial translocation.
Main Results:
- CD101 expression on myeloid cells and T lymphocytes confers protection against experimental enterocolitis and T1D.
- Reduced CD101 expression is observed in patients with T1D and IBD.
- Distinct bacteria and inflammation suppress CD101 expression on immune cells.
Conclusions:
- Reduced CD101 expression in T1D and IBD patients may result from gut dysbiosis and bacterial translocation.
- This reduction could contribute to heightened inflammatory immune responses in these conditions.
- Targeting host-microbiota interactions and CD101 expression may offer therapeutic strategies for IBD and T1D.


