2017 Fiscal Year Final Research Report
Why does Stevens-Johnson syndrome develop with mycoplasma pneumonia?
| Project/Area Number |
15K09781
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Dermatology
|
|---|
| Research Institution | Kyorin University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Keywords | アレルギー / 感染症 / 薬疹 / 制御性T細胞 / SJS |
|---|
| Outline of Final Research Achievements |
Although the relation of Stevens-Johnson syndrome (SJS) and Mycoplasma pneumoniae (MP) infection has been well known, it remains unknown how MP infection contributes to SJS development. We investigated the frequencies and phenotype of regulatory T cells (Treg) in the peripheral blood of MP infection and viral infections patients at onset and after clinical resolution, and healthy controls.
The functional Treg was significantly decreased not only in the acute but also resolution stage of MP infection. IL-17A+Foxp3+ T cells was significantly increased in the resolution stage of MP infection. The development of IL-17A+Foxp3+ cells were found to be dependent on the generation of the ‘pathogenic’ pMOs, which are characterized by the potential to abundantly produce IL-6 in a TLR-2-dependent manner. Our findings suggest that MP infections could serve to enhance the risk of subsequently developing severe allergic diseases by chronically abrogating Treg-mediated suppression.
|
| Free Research Field |
皮膚科学
|
