1999 Fiscal Year Final Research Report Summary
The development and activation of MHC class II-restricted Blymphocytes.
| Project/Area Number |
09470094
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | Osaka University |
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Principal Investigator |
HAMADKA Toshiydki Graduate School of Medicine, Osaka University Professor, 医学系研究科, 教授 (60028529)
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| Co-Investigator(Kenkyū-buntansha) |
ONO Shiro Grad. Sch Med., Osaka Univ. Associate Professor, 医学系研究科, 助教授 (80127208)
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| Project Period (FY) |
1997 – 1999
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| Keywords | Ia-restriction / B-cell differentiation / polyclonal IgM production / B-B cell interaction / LPS / Ia-deficient mice / Ig transgenic mice |
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| Research Abstract |
We have provided evidence supporting that self-I-A-restricted B-B cell interaction is involved in the PBA (polyclonal B-cell activator)-induced polyclonal differentiation of murine resting B cells into IgM-producing cells. In addition, experiments using double bone marrow chimeras have revealed that the I-A-restriction specificity is dictated by the Ia haplotype of bone marrow cells present during the B cell ontogeny but not by the Ia haplotype of a radiation-resistant host environment.
In the present study, utilizing Ia-deficient and Ig-transgenic mice we examined mechanisms by which I-A-restricted B cells are generated and activated. It was demonstrated that B cells from Ia-deficient mice are defective in LPS-induced polyclonal IgM Ab responses, but when Ia-deficient mice are neonatally administrated Ia-positive B cells as educator cells, the B cells become responsive to LPS in the presence of the Ia-expressing B cells as auxiliary cells almost the same as normal B cells. This suggests that I-A-restricted B-B cell interaction is mediated by non-Ia and Ia molecules. Moreover, B cells with monoclonal specificity obtained from Ig-transgenic mice failed to exhibit IgM Ab responses to LPS, indicating a possible involvement of sIg in the self-Ia recognition by responding B cells through non-Ia molecules.
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