Study on self recognition system of T lymphocytes and structural analysis of TCR : CD3 Complex

T淋巴细胞自我识别系统研究及TCR：CD3复合物结构分析

• 批准号: 63480163
• 负责人: ONOE Kazunori
• 金额: $ 4.1万
• 依托单位: Hokkaido University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (B)
• 财政年份: 1988
• 资助国家: 日本
• 起止时间: 1988 至 1989
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-63480163/
• 关键词: Bone marrow chimera; Thymocytes differentiation; Self recognition; Positive selection; Induction of self-tolerance; TCR; Negative selection; T細胞抗原レセプター

1) We found that development of signal transduction system of T cells as well as selection of T cell repertoire were controlled by thymic stroma.2) We analyzed differentiation process of thymocytes from allogeneic bone marrow chimera mice and found that the process was much more complex that had been thought.3) We identified strcmal cells that were essential in inducing self-tolerance. The most important cells were Ia^+ macrophages or dendritic cells in the thymic medulla.4) We found that acute GVHR occurred in the thymus. The GVHR eventually abrogated the induction system of self tolerance in the thymus.5) We identified precise location on H-2 class I molecules that was involved in positive selection of T cell repertoire.6) We identified precise location on H-2 class II molecules that was involved in self class II-restricted recognition of synthetic peptide antigens. The location was well-preserved among different H-2 class II molecules.

1）我们发现，T细胞的信号转导系统的发展以及T细胞库的选择受胸腺基质的控制。2）我们分析了来自同种异体骨髓嵌合体的胸腺细胞的分化过程，并发现该过程更为复杂。最重要的细胞是胸腺髓质中的Ia^+巨噬细胞或树突状细胞。4）我们发现胸腺中发生急性GVHR。 GVHR最终废除了胸腺中自耐力的诱导系统。5）我们在H-2 I类分子上确定了与T细胞库阳性选择的H-2 I类分子的精确位置。6）6）我们确定了H-2 II类分子上的精确位置，该位置参与了自我II类II级限制性限制性识别合成肽抗生素的分子。该位置在不同的H-2 II类分子中保存得很好。

项目成果

Onoe,Kazunori: "Donor and recipient specific tolerance in cells from semi-allogeneic,H-2 subregion compatible or fully allogeneic bone marrow chimeras attributable to clonal deletion" Immunobiol.179. 172-189 (1989)

Onoe，Kazunori：“来自半同种异体、H-2 亚区相容或完全同种异体骨髓嵌合体的细胞中供体和受体特异性耐受可归因于克隆缺失”Immunobiol.179。

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Onoe,Kazunori: Acta Pathol.Jpn.38. 101-110 (1989)

Onoe，Kazunori：Acta Pathol.Jpn.38。

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