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Updated: Sep 29, 2025

Microbiota Analysis Using Two-step PCR and Next-generation 16S rRNA Gene Sequencing
Published on: October 15, 2019
Microbiota, IgA and Multiple Sclerosis
Léo Boussamet1, Muhammad Shahid Riaz Rajoka2, Laureline Berthelot1
1Centre for Research in Transplantation and Translation Immunology, Nantes Université, Inserm, CR2TI UMR, 1064 Nantes, France.
Abstract:
Multiple sclerosis (MS) is a neuroinflammatory disease characterized by immune cell infiltration in the central nervous system and destruction of myelin sheaths. Alterations of gut bacteria abundances are present in MS patients. In mouse models of neuroinflammation, depletion of microbiota results in amelioration of symptoms, and gavage with MS patient microbiota exacerbates the disease and inflammation via Th17 cells. On the other hand, depletion of B cells using anti-CD20 is an efficient therapy in MS, and growing evidence shows an important deleterious role of B cells in MS pathology. However, the failure of TACI-Ig treatment in MS highlighted the potential regulatory role of plasma cells. The mechanism was recently demonstrated involving IgA+ plasma cells, specific for gut microbiota and producing IL-10. IgA-coated bacteria in MS patient gut exhibit also modifications. We will focus our review on IgA interactions with gut microbiota and IgA+ B cells in MS. These recent data emphasize new pathways of neuroinflammation regulation in MS.
Insights
Multiple sclerosis (MS) involves gut bacteria and immune cells. IgA+ plasma cells producing IL-10 may regulate gut microbiota, offering new insights into neuroinflammation in MS.
Area of Science:
- Neuroimmunology
- Microbiome research
- Autoimmune diseases
Background:
- Multiple sclerosis (MS) is a neuroinflammatory disease affecting the central nervous system.
- Gut microbiota alterations are observed in MS patients, influencing disease severity.
- B cells play a role in MS pathology, but their precise function, especially plasma cells, is complex.
Purpose of the Study:
- To review the interaction between immunoglobulin A (IgA), gut microbiota, and IgA+ B cells in MS.
- To explore the regulatory role of IgA+ plasma cells in MS pathogenesis.
- To highlight novel pathways in neuroinflammation regulation.
Main Methods:
- Literature review focusing on IgA, gut microbiota, and B cells in MS.
- Analysis of studies on microbiota transplantation and B cell depletion therapies.
- Examination of mechanisms involving IgA+ plasma cells and IL-10 production.
Main Results:
- Gut microbiota composition is altered in MS patients.
- IgA+ plasma cells producing IL-10, specific for gut microbiota, may have a regulatory role.
- IgA coating of bacteria is modified in the gut of MS patients.
Conclusions:
- IgA interactions with gut microbiota and IgA+ B cells represent a significant pathway in MS neuroinflammation.
- Understanding these interactions may reveal new therapeutic targets for MS.
- The role of plasma cells in MS warrants further investigation, particularly their immunomodulatory functions.
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