| Project/Area Number |
03454179
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
寄生虫学(含医用動物学）
|
|---|
| Research Institution | Jikei University School of Medicine |
|---|
Principal Investigator |
WATANABE Naohiro Jikei University School of Medicine Department of Parasitology, Associate Professor, 医学部, 助教授 (00057019)
|
|---|
| Project Period (FY) |
1991 – 1992
|
| Project Status |
Completed (Fiscal Year 1992)
|
| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1992: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1991: ¥2,000,000 (Direct Cost: ¥2,000,000)
|
|---|
| Keywords | IgE / Eosinophilia / Parasite / Protective immunity / Helminth / Schistosoma / Trichinella / Mast cell / 高IgE血症 / マレー糸状虫 / 糞線虫 / コスタリカ住血線虫 / 好酸球 |
|---|
| Research Abstract |
The aim of study is to know the effects of IgE on eosinophilia and protective immunity in the host with helminth infections. The experiments were performed selective IgE-deficient and IgE-producing control mice. Anti-helminth IgE antibody had protective roles in expulsion of Hymenolepis nana, resistance to muscle larvae of Trichinella spiralis and egg-granuloma formation of Schistosoma japonicum. IgE antibody dependency of protective immunity was found especially in the host expressing high IgE response. However, IgE antibody was not essential factor for protective immunity. Because, protection was demonstrated in IgE-deficient mice.
In the infection of Brugia malayi, Strongyloides ratti, Angiostrongylus costaricensis and Nippostrongylus brasiliensis, IgE production enhanced 10-50 times by the infection. The enhanced IgE had no binding activity to helminth antigens. This nonspecific IgE did not have direct protective role. On the other hand, the protective activity by anti-helminth IgE antibody reduced in mice with hyper IgE obtained by transferring large amount of nonspecific IgE or by Nippostrongylus infection. These results suggest that nonspecific IgE makes establishment of infection easier through interference to the IgE antibody dependent protective immunity. This is an escape mechanism of parasites from host protection.
It was unlikely that anti-helminth IgE antibody and nonspecific IgE played a role in the induction of eosinophilia in the present experiments. The main factor for eosinophilia seems to be IL-5 derived from T cells induced by helminth infections.
|
