| Project/Area Number |
04454070
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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 |
応用生物化学・栄養化学
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| Research Institution | The University of Tokyo |
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Principal Investigator |
KAMINOGAWA Shuichi The University of Tokyo Faculty of Agriculture Professor, 農学部, 教授 (50011945)
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| Project Period (FY) |
1992 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 1994: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1993: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1992: ¥3,400,000 (Direct Cost: ¥3,400,000)
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| Keywords | Immunoglobulin gene / Antibody Production / B cell / Peptide / beta-lacreglobulin / Food allevgy / MHC クラス II 分子 / T細胞膜成分 / IgE / クラススイッチ / ペプチド免疫 / IgM産生B細胞クローン / B細胞ハイブリドーマ / gene usage / パラトープ構造 |
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| Research Abstract |
To elucidate the molecular and cellular mechanism of lgE-class switching leading to allergic diseases, we examined the differentiation process of antigen-specific B cells at a clonal level in related to the repertoire of helper T cells. We used a peptide fragment encompassing residues 25-40 (F25-40) of beta-lactoglobulin, which contained B cell determinant. T cell repertoire collaborating with F25-40-specific B cell were modified by priming with 1) beta-LG,2) F25-40-conjugated carrier protein or 3) F21-40. Thus, we demonstrate the helper functions of T cells in B cells differentiation at a clonal level by comparing primed B cell repertoire, class switching or affinity maturation among priming antigens. Consequently, the immunization with F21-40 could not induce strong lgG-class II switching. In addition, the restricted V_H gene usage (J558) was observed among B cell repertoire elicited by F21-40 distinct from other antigens. From these results, it has been suggested that T cell repertoire collaborating with B cells restrict B cell repertoire differentiating into Ab-secreting cells. To determine the molecular mechanism of the restriction, we analyzed the exact roles of the interaction between MHC class II molecules and T cell receptor on B cell activation. The results showed that the class II-mediated signals directly activate B cells and enhance lgG production. From these results, it has been suggested that the class II-mediated signals play an important role on the restriction of B cell repertoire and class switching.
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