2017 Fiscal Year Final Research Report
Study on immunological mechanism for high pathogenicity of Cryptococcus gattii infection
| Project/Area Number |
15H04867
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Infectious disease medicine
|
|---|
| Research Institution | Tohoku University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Renkei-kenkyūsha) |
ISHII KEIKO 東北大学, 大学院医学系研究科, 准教授 (00291253)
|
|---|
| Project Period (FY) |
2015-04-01 – 2018-03-31
|
| Keywords | クリプトコックス・ガッティ / 高病原性 / 免疫機序 / トランスジェニックマウス |
|---|
| Outline of Final Research Achievements |
Cryptococcus gattii causes meningoencephalitis leading to high fatality rate even in healthy individuals without immunodeficiency, which is contrary to C. neoformans. In this study, to clarify the mechanism for high pathogenicity of C. gattii infection, we addressed the possible difference in host immune response to these fungal species. Th1 immune response was attenuated in the lungs of mice infected with C. gattii, which was associated with impaired Th1 cell differentiation. In addition, different responsiveness mediated by TLR9 and Dectin-2, critical processes for Th1 cell differentiation from antigen-specific naive T cells, was found in DNA and capsular polysaccharides from C. gattii and C. neoformans. These results suggest that distinct PAPMs structures leading to lowered Th1 immune response may be involved in the high virulence of C. gattii.
|
| Free Research Field |
感染免疫学
|
