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大鼠T淋巴细胞来源的IgE结合因子的调节作用。I. IgE增强因子增强IgE反应的机制。

Regulatory role of IgE-binding factors from rat T lymphocytes. I. Mechanism of enhancement of IgE response by IgE-potentiating factor.

作者信息

Suemura M, Yodoi J, Hirashima M, Ishizaka K

出版信息

J Immunol. 1980 Jul;125(1):148-54.

PMID:6966648
Abstract

T lymphocytes in the mesenteric lymph nodes of rats infected with Nippostrongylus brasiliensis spontaneously released a soluble factor that selectively potentiated the IgE-forming cell response of antigen-primed cells to homologous antigen. The factor could enhance the IgE response of DNP-OA-primed cells to DNP-HSA and T cell-replacing factor. In contrast, the treatment of OA-primed T cells with the factor failed to enhance either the IgE or IgG response of the mixture of DNP-KLH primed cells and OA-primed T cells to DNP-OA. The results collectively suggested that the target cells of the IgE-potentiating factor are B cells. Indeed, IgE potentiating factor was absorbed by B cells rather than T cells or thymocytes. Evidence was obtained that IgE-potentiating factor could be absorbed by IgE-bearing B cells or IgE-coupled Sepharose, indicating that the factor had affinity for IgE. It appeared that the potentiating factor bound to IgE-bearing B cells and selectively enhanced the differentiation of IgE-B cells to IgE-forming cells. It was also found that the major source of the factor was Fc epsilon R-bearing T cells.

摘要

感染巴西日圆线虫的大鼠肠系膜淋巴结中的T淋巴细胞自发释放一种可溶性因子,该因子能选择性增强经抗原致敏的细胞对同源抗原的IgE形成细胞反应。该因子可增强经二硝基苯酚 - 卵清蛋白(DNP - OA)致敏的细胞对二硝基苯酚 - 人血清白蛋白(DNP - HSA)和T细胞替代因子的IgE反应。相比之下,用该因子处理经卵清蛋白(OA)致敏的T细胞,未能增强经二硝基苯酚 - 钥孔血蓝蛋白(DNP - KLH)致敏的细胞与经OA致敏的T细胞混合物对DNP - OA的IgE或IgG反应。这些结果共同表明,IgE增强因子的靶细胞是B细胞。事实上,IgE增强因子被B细胞而非T细胞或胸腺细胞吸收。有证据表明,IgE增强因子可被携带IgE的B细胞或IgE偶联的琼脂糖吸附,这表明该因子对IgE具有亲和力。似乎该增强因子与携带IgE的B细胞结合,并选择性增强IgE - B细胞向IgE形成细胞的分化。还发现该因子的主要来源是携带FcεR的T细胞。

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