Kimoto M, Krenz T J, Fathman C G
J Exp Med. 1981 Sep 1;154(3):883-91. doi: 10.1084/jem.154.3.883.
Long-term-cultured poly(Tyr, Glu)-poly-D,L,-Ala-poly-Lys [(T,G)-A--L]-reactive T cells and clones derived from (high responder x low responder)F1 [(C57BL/6 x A/J)F1] mice were shown to recognize (T,G)-A--L presented by cells from low responder strain A/J mice. The antigen-presenting determinant(s) that allowed recognition of (T,G)-A--L by such T cell clones was controlled by the I-A subregion of the major histocompatibility complex. These results suggest that there is no functional defect in the ability of low responder Ir gene products (I-A antigens) to associate with (T,G)-A--L for effective recognition by T cells. Although these results might tentatively be interpreted to suggest that Ir gene-controlled low responsiveness is due to the inability of the T cell to recognize the association between (T,G)-A--L and low responder I-A gene products, it is similarly possible that there might be a defect in the functional capabilities of low responder antigen-presenting cells to effectively process (T,G)-A--L into immunodominant epitopes.
长期培养的聚(酪氨酸,谷氨酸)-聚-D,L-丙氨酸-聚赖氨酸[(T,G)-A-L]反应性T细胞以及源自(高反应性×低反应性)F1[(C57BL/6×A/J)F1]小鼠的克隆被证明能够识别低反应性品系A/J小鼠细胞所呈递的(T,G)-A-L。此类T细胞克隆识别(T,G)-A-L的抗原呈递决定簇由主要组织相容性复合体的I-A亚区控制。这些结果表明,低反应性Ir基因产物(I-A抗原)与(T,G)-A-L结合以供T细胞有效识别的能力不存在功能缺陷。尽管这些结果可能初步被解释为表明Ir基因控制的低反应性是由于T细胞无法识别(T,G)-A-L与低反应性I-A基因产物之间的结合,但同样有可能低反应性抗原呈递细胞将(T,G)-A-L有效加工成免疫显性表位的功能能力存在缺陷。