1990 Fiscal Year Final Research Report Summary
IMMUNOLOGICAL AND GENETIC STUDY ON IgEFc RECEPTOR IN PATIENTS WITH ATOPIC BRONCHIAL ASTHMA
| Project/Area Number |
01480232
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | HOKKAIDO UNIVERSITY |
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Principal Investigator |
KAWAKAMI Yoshikazu HOKKAIDO UNIVERSITY SCHOOL OF MEDICINE, PROFESSOR, 医学部, 教授 (10001877)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGUCHI Etsuro HOKKAIDO UNIVERSITY MEDICAL HOSPITAL, INSTRUCTOR, 医学部附属病院, 助手 (10201831)
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| Project Period (FY) |
1989 – 1990
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| Keywords | Atopic bronchial asthma / IgE / IgEFc receptor / Linkage analysis |
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| 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
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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
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