| Project/Area Number |
63570230
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Immunology
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| Research Institution | HYOGO COLLEGE OF MEDICINE |
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Principal Investigator |
HAMANO Teruaki HYOGO COLLEGE OF MEDICINE, THE 2ND DEPARTMENT OF INTERNAL MEDICINE, LECTURER, 医学部, 講師 (40068515)
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| Co-Investigator(Kenkyū-buntansha) |
IWASAKI Tsuyoshi HYOGO COLLEGE OF MEDICINE, THE 2ND DEPARTMENT OF INTERNAL MEDICINE, ASSISTANT PR, 医学部, 助手 (10151721)
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| Project Period (FY) |
1988 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1989: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1988: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | TNP-SPECIFIC B CELL CLONE / B CELL DIFFERENTIATION / ANTI-TNP PEC / MHC CLASS 2 MOLECULE / CELL FUSION / TNP-RFC / 抗原特異的B細胞クロ-ン / MHCクラスII抗原 / TNP-BSA / TNP基特異的B細胞クローン / 抗TNP抗体産生細胞 / TNP化抗原 / r-IL5 |
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| Research Abstract |
TP67.14 is a subclone of a resulting B cell hybridoma established by somatic hybridization between splenic B cells of A/J mice immunized with TNP-LPS and 2.52 M, a HAT medium-sensitive mutant of a B cell line: it expresses IgM, B220, IA^k, and IE^k on the cell membrane and also possesses a receptor molecule for TNP on its surface derived from TNP-reactive B cells of A/J mice used for cell fusion. As shown previously, TP67.14 could be induced to generate a significant amount of anti-TNP antibodies when treated with TNP-conjugated protein such as TNP-BSA and TNP-keyhole limpet hemocyanin without T cell help as well as LPS.
Our study was under-taken to investigate direct involvement of surface MHC class II molecules on B cells dering B cell maturation by analysis with this Ag-specific B cell clone. The data demonstrate that mAb against IA^k and IE^k molecules, but not IA^d and H-2^k, markedly inhibited the differentiative effects of LPS on TP67.14/ In contrast, both antibodies specifically augmented the secretion of anti-TNP antibodies by TP67.14 treated with TNP-BSA, although these antibodies alone failed to induce the generation of anti-TNP antibodies Interestingly, YP67.14 significantly differentiated into anti-TNP antibody secreting cells when incubated with TNP-conjugated monoclonal anti-IA^k or anti-IE^k antibodies alone; this differentiative effect was much greater than that of TNP-conjugated anti-IA^d mAb or purified mouse IgG under the same conditions.
Our result suggests that surface IA/E molecules on B cells may be directly involved in a transductional signal for B cell maturation mediated by the cross-linkage of receptor molecules on B cells with Ag.
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