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Updated: Dec 8, 2025
Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
Monocyte-Independent and -Dependent Regulation of Regulatory T-Cell Development in Mycoplasma Infection
Ryo Takahashi1, Tetsuo Shiohara1,2, Yoshiko Mizukawa2
1Flow Cytometry Core Facility, Kyorin University Graduate School of Medicine, Mitaka, Tokyo, Japan.
Background:
Although Mycoplasma pneumoniae (MP) infection has been implicated in the pathogenesis of allergic diseases, the mechanism of this trigger remains unknown. We explored the mechanism for how MP infection could tilt the balance between regulatory T cells (Tregs) and Th17 cells.
Methods:
We analyzed the frequency, phenotype, and function of Tregs in patients at the different stages of MP and various virus infections over a period of more than 1 year. We examined the effect of monocytes to elucidate signals that can regulate the balance between Treg and Th17 cells.
Results:
The functional activity of Tregs was profoundly impaired during the acute stage of MP as well as viral infections. Upon resolution, however, the Treg function remained impaired even 1 year after MP infection. In the resolution stage, the impaired Treg function was associated with an increase in interleukin (IL) 17A+ Tregs and Th17 cells. Development of Th17 cells was dependent on the "aberrant" proinflammatory monocytes (pMOs), characterized by potent ability to produce IL-6 in a Toll-like receptor 2-dependent manner.
Conclusions:
Depending on the prevalence of the pMOs, Tregs and Th17 cells could mutually regulate the number and function of the other. The pMOs/IL-6 could be crucial therapeutic targets against MP-induced allergic diseases.
Insights
Mycoplasma pneumoniae infection impairs regulatory T cell function long-term, promoting Th17 cells via proinflammatory monocytes. Targeting these monocytes and IL-6 may prevent MP-induced allergic diseases.
Area of Science:
- Immunology
- Microbiology
- Allergy Research
Background:
- Mycoplasma pneumoniae (MP) infection is linked to allergic diseases, but the underlying mechanism is unclear.
- This study investigates how MP infection disrupts the balance between regulatory T cells (Tregs) and Th17 cells.
Purpose of the Study:
- To explore the mechanism by which MP infection influences Treg and Th17 cell populations.
- To identify key cellular and molecular signals regulating Treg/Th17 balance during MP infection.
Main Methods:
- Analysis of Treg frequency, phenotype, and function in patients with MP and viral infections over one year.
- Investigation of monocyte-derived signals impacting Treg and Th17 cell differentiation and function.
Main Results:
- Treg function was significantly impaired during acute MP infection and remained impaired for up to one year post-infection.
- Impaired Treg function correlated with increased interleukin (IL)-17A+ Tregs and Th17 cells during the resolution phase.
- Th17 cell development was dependent on "aberrant" proinflammatory monocytes (pMOs) producing IL-6 via Toll-like receptor 2.
Conclusions:
- Proinflammatory monocytes (pMOs) and IL-6 play a critical role in modulating Treg and Th17 cell populations during MP infection.
- pMOs and IL-6 represent potential therapeutic targets for preventing or treating MP-induced allergic diseases.
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