HLA-linked nonresponsiveness to Cryptomeria japonica pollen antigen. I. Nonresponsiveness is mediated by antigen-specific suppressor T cell.
HLA-linked nonresponsiveness to Cryptomeria japonica pollen antigen. I. Nonresponsiveness is mediated by antigen-specific suppressor T cell.
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HLA 相关性对柳杉花粉抗原无反应。
DOI：
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发表时间：
1987
影响因子：
4.4
通讯作者：
Takehiko Sasazuki
中科院分区：
文献类型：
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作者：
Sho Matsushita;Masahiko Muto;M. Suemura;Y. Saito;Takehiko Sasazuki
本研究的目的是阐明IgE对Cryptomeria japonica （Japanese cedar）花粉抗原（CPAg）无应答的细胞机制，我们之前的研究显示CPAg是hla连锁的(1)。我们建立了一个抗原特异性和同型特异性的检测系统，用于检测少量抗cpag IgE抗体，并建立了一个体外诱导抗原驱动IgE抗体合成的培养系统。通过这些方法，我们阐明了HLA-DR分子在CPAg驱动的IgE反应中的作用类似于小鼠体内的I-A或I-E分子，即免疫反应基因（Ir-genes）的产物，因为抗HLA-DR单克隆抗体阻断了应答，单核细胞和单核细胞耗尽的外周血淋巴细胞（PBL）对CPAg应答的相互作用受到HLA-DR的限制。此外，当Leu-2+3- T细胞片段减少时，无应答者的PBL显示出对CPAg的特异性IgE反应，从而表明即使无应答者也具有CPAg特异性的Leu-2-3+ T细胞和B细胞克隆，并且由于CPAg特异性的Leu-2+3-抑制T细胞的存在，它们显然没有反应。这种抑制性T细胞部分以cpag特异性的方式消除了自体B +单核细胞+ Leu-2-3+ T细胞的IgE反应。目前的细胞分析和我们之前的遗传分析强烈表明，hla相关的IgE对CPAg的无反应是由CPAg特异性抑制T细胞介导的。因此，控制对CPAg无反应的hla连接基因被指定为CPAg的免疫抑制基因（is -CPAg）。讨论了HLA-DQ子区域内is - cpag的定位。
The objective of this study was to elucidate the cellular mechanism of IgE nonresponse to the Cryptomeria japonica (Japanese cedar) pollen antigen (CPAg), which was shown in our previous study to be HLA-linked (1). We established an assay system for the measurement of small amounts of anti-CPAg IgE antibody, both in an antigen-specific and isotype-specific manner, and a culture system to induce antigen-driven IgE antibody synthesis in vitro. By using these methods, we clarified that the function of the HLA-DR molecule in the CPAg-driven IgE response is similar to that of I-A or I-E molecule in mice, namely the product of immune response genes (Ir-genes), because anti-HLA-DR monoclonal antibody blocked the response, and the interaction between monocyte and monocyte-depleted peripheral blood lymphocytes (PBL) to respond to CPAg was restricted by HLA-DR. Furthermore, PBL from nonresponders revealed a specific IgE response to CPAg when the Leu-2+3- T cell fraction was depleted, thereby suggesting that even nonresponders have Leu-2-3+ T cell and B cell clones specific for CPAg, and they apparently show no response due to the presence of CPAg-specific Leu-2+3- suppressor T cells. This suppressor T cell fraction abolished the IgE response of the autologous B + monocyte + Leu-2-3+ T cell in a CPAg-specific manner. The current cellular analysis together with our previous genetic analysis strongly suggest that the HLA-linked IgE nonresponse to CPAg is mediated by CPAg-specific suppressor T cells. The HLA-linked gene controlling the nonresponsiveness to CPAg is thus designated as the immune suppression gene for CPAg (Is-CPAg). Mapping of Is-CPAg within HLA-DQ subregion is discussed.