Durum S K, Higuchi C, Ron Y
Immunobiology. 1984 Dec;168(3-5):213-31. doi: 10.1016/S0171-2985(84)80112-6.
Accessory cells are required for the activation of helper T cells. We have examined two characteristics of accessory cells, their expression of I-A, and their ability to release IL1. We provide evidence that these two properties are related, and postulate that membrane I-A molecules participate in the pathway leading to IL1-release. Experimental results are described relating I-A to IL1-release as follows: 1. In vitro-educated Ly1 T cells stimulate IL1-release from M phi; this process is H-2-restricted and blocked by anti-I-A antibodies. 2. H-2-restriction between T cells and M phi is overcome in the presence of ConA, but this unrestricted interaction is also blocked by anti-I-A. 3. LPS stimulation of IL1-release is blocked by anti-I-A. These findings suggested an active role for I-A molecules on IL1-producing cells. We next describe a series of experiments designed to assess the requirements for I-A versus IL1 during T cell activation. In a number of experimental systems, T cells demonstrated a requirement for I-A-recognition, but none that could not also be satisfied by IL1: 1. Generation of helper T cells in allogeneic chimeras. 2. Proliferation of KLH-primed lymph node cells. 3. Proliferation of KLH-primed lymph node cells from chronically anti-I-A-suppressed mice. 4. Proliferation of GAT-primed lymph node cells from nonresponder mice. These findings suggest that for many kinds of T cells (not necessarily all) the apparent requirement for I-A-recognition is primarily involved in stimulating IL1-release from accessory cells.
辅助性T细胞的激活需要辅助细胞。我们研究了辅助细胞的两个特性,即它们I-A分子的表达以及释放白细胞介素1(IL1)的能力。我们提供的证据表明这两个特性是相关的,并推测膜I-A分子参与了导致IL1释放的途径。现将I-A与IL1释放相关的实验结果描述如下:1. 体外培养的Ly1 T细胞刺激巨噬细胞释放IL1;这个过程受H-2限制,并被抗I-A抗体阻断。2. 在刀豆蛋白A(ConA)存在的情况下,T细胞与巨噬细胞之间的H-2限制被克服,但这种无限制的相互作用也被抗I-A阻断。3. 脂多糖(LPS)刺激IL1释放被抗I-A阻断。这些发现表明I-A分子在产生IL1的细胞上发挥着积极作用。接下来我们描述一系列旨在评估T细胞激活过程中对I-A与IL1需求的实验。在许多实验系统中,T细胞表现出对I-A识别的需求,但所有这些需求也都可以通过IL1来满足:1. 同种异体嵌合体中辅助性T细胞的产生。2. 钥孔血蓝蛋白(KLH)致敏的淋巴结细胞的增殖。3. 来自长期抗I-A抑制小鼠的KLH致敏的淋巴结细胞的增殖。4. 来自无反应小鼠的谷氨酸-丙氨酸-酪氨酸(GAT)致敏的淋巴结细胞的增殖。这些发现表明,对于许多类型的T细胞(不一定是所有T细胞)而言,对I-A识别的明显需求主要是为了刺激辅助细胞释放IL1。