| Project/Area Number |
01480232
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Respiratory organ internal medicine
|
|---|
| Research Institution | HOKKAIDO UNIVERSITY |
|---|
Principal Investigator |
KAWAKAMI Yoshikazu HOKKAIDO UNIVERSITY SCHOOL OF MEDICINE, PROFESSOR, 医学部, 教授 (10001877)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
YAMAGUCHI Etsuro HOKKAIDO UNIVERSITY MEDICAL HOSPITAL, INSTRUCTOR, 医学部附属病院, 助手 (10201831)
|
|---|
| Project Period (FY) |
1989 – 1990
|
| Project Status |
Completed (Fiscal Year 1990)
|
| Budget Amount *help |
¥6,400,000 (Direct Cost: ¥6,400,000)
Fiscal Year 1990: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1989: ¥4,900,000 (Direct Cost: ¥4,900,000)
|
|---|
| Keywords | Atopic bronchial asthma / IgE / IgEFc receptor / Linkage analysis / 気管支喘息 / アトピ- / Fcリセプタ- / 気管支肺胞洗浄 |
|---|
| Research Abstract |
We investigated the expression of low affinity receptor for IgE Fc portion (Fc epsilon R II), which plays a major roles in atopic bronchial asthma. An increase in the intensity of expression of Fc epsilon R II and the proportion of cells bearing thi13EA\ : s antigen was observed for peripheral B cells in atopic bronchial asthma. In contrast, no such heightened expression was observed for T cells both in peripheral blood and bronchoalveolar lavage fluid. Levels of soluble Fc epsilon R II) were not incr13EA\ : eased in patients' serum. Patients with pulmonary sarcoidosis, who had increased serum levels of interferon-gamma which competed with IL-4 in regulatory roles of Fc epsilon R II, did not show decreased serum Fc epsilon R II levels. Thus, these resul13EA\ : ts suggest that membrane-bound Fc epsilon R II (mFc epsilon R II) on B cell surface is more appropriate than sFc epsilon R II as a marker of type I allergic reaction.
We next cultured peripheral blood B cells in vitro in the prese
… More
nce of IL-4 and examined the expression of mFc epsilon R II and production of sFc epsilon R II.No significant difference in these parameters was observed between normal subjects and pat13EA\ : ients with atopic bronchial asthma or pulmonary sarcoidosis. Accordingly, it seemed that the increased expression of Fc epsilon R II in fresh B cells was not due to inherent alterations in IL-4-responsiveness of atopic patients.
To search for a locus of gene responsible for atopy defined as hightened state of lgE production, we examined linkage between atopy and locus 11q13, using restriction fragment length polymorphism (RFLP) of a marker DNA.No significant linkage was fo13EA\ : und for 58 members from 4 families which included a atopic patient as a proband, which sharply contradicted the previous report from Britain. Thus, our study failed to confirm the notion that a gene at locus 11q13 or near this locus determined atopy13EA\ : . However, the presence of one of 5 alleles detected by the same DNA probe was significantly associated with high serum IgE, thus suggesting that some gene at/near this locus was partially responsible for appearance of atopy. Less
|
