Rademaekers A, Kölsch E
Institut für Immunologie, Universität Münster, Germany.
Eur J Immunol. 1995 Feb;25(2):623-6. doi: 10.1002/eji.1830250247.
The isotype expression in the J558 idiotype-associated humoral immune response against alpha(1-->3)-dextran in BALB/c mice is controlled by idiotype-specific T cells which silence in situ B lymphocytes primed and committed to an IgG response. This leads to a restriction of the type II thymus-independent response to the sole production of IgM antibodies. The availability of the T cell receptor (TcR) alpha and beta sequences for such a regulatory T cell clone allows the investigation of the degree of heterogeneity of the TcR usage of these T cells. It is found that all alpha(1-->3)-dextran-primed BALB/c mice use a very similar, possibly identical TcR. This suggests a tight, possibly genetically programmed, interaction between the J558 idiotype-bearing dextran-specific B cells and their idiotype-specific regulatory T cell counterparts.
BALB/c小鼠针对α(1→3)-葡聚糖的J558独特型相关体液免疫应答中的同种型表达,由独特型特异性T细胞控制,这些T细胞使已启动并倾向于产生IgG应答的原位B淋巴细胞沉默。这导致II型非胸腺依赖性应答局限于仅产生IgM抗体。此类调节性T细胞克隆的T细胞受体(TcR)α和β序列的可得性,使得对这些T细胞TcR使用的异质性程度进行研究成为可能。研究发现,所有经α(1→3)-葡聚糖启动的BALB/c小鼠都使用非常相似、可能相同的TcR。这表明携带J558独特型的葡聚糖特异性B细胞与其独特型特异性调节性T细胞对应物之间存在紧密的、可能是基因编程的相互作用。