REVERSAL OF INVITRO T-CELL CLONAL ANERGY BY IL-2 STIMULATION
REVERSAL OF INVITRO T-CELL CLONAL ANERGY BY IL-2 STIMULATION
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DOI：
10.1093/intimm/4.6.661
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发表时间：
1992-06-01
影响因子：
4.4
通讯作者：
SCHWARTZ, RH
中科院分区：
文献类型：
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作者：
BEVERLY, B;KANG, SM;SCHWARTZ, RH
在体外用伴刀豆球蛋白A在不存在抗原呈递细胞（APC）的情况下刺激正常I型小鼠T辅助细胞克隆（T（H）1）导致被称为T细胞克隆无反应性的低应答状态的诱导。 这种状态的特征在于用抗原和APC刺激后增殖的减少，这是由于IL-2的产生减少。 淋巴因子IL-3/粒细胞巨噬细胞集落刺激因子和IFN-γ的产生也减少，尽管程度较低。 用IL-2刺激这种无反应性细胞导致增殖和状态的完全逆转。 我们证明，这种逆转不是由于逃避无反应诱导的细胞亚群的生长，而是发生在所有细胞中。 无反应性也自发消散，虽然慢得多，在T细胞抗原受体占用的情况下。 最后，我们表明，如果在16-20 h去除IL-2和其他因子，抗原和APC的正常激活可以产生类似的状态。 这些结果表明，无能状态不是T（H）1细胞的永久性变化。 无反应性诱导似乎是细胞在通过抗原特异性受体刺激后不能广泛分裂的结果。 我们提出了一个模型来解释这些结果的一个相对稳定的负调控因子。
Stimulation of a normal type I mouse T helper cell clone (T(H)1) with concanavalin A in the absence of antigen presenting cells (APC) in vitro results in the induction of a hyporesponsive state known as T cell clonal anergy. This state is characterized by a decrease in proliferation following stimulation with antigen and APC resulting from a decrease in the production of IL-2. Production of the lymphokines IL-3/granulocyte macrophage colony stimulating factor and IFN-gamma is also reduced, although to a lesser degree. Stimulation of such anergic cells with IL-2 results in proliferation and a complete reversal of the state. We demonstrate that this reversal is not due to the outgrowth of a subpopulation of cells that had escaped anergy induction, but rather occurs in all the cells. Anergy also dissipated spontaneously, although much more slowly, in the absence of T cell antigen receptor occupancy. Finally, we show that a similar state can be produced by normal activation with antigen and APC if IL-2 and other factors are removed at 16-20 h. These results indicate that the anergic state is not a permanent change in the T(H)1 cell. Anergy induction appears to be a consequence of the inability of the cell to divide extensively following stimulation through the antigen-specific receptor. We propose a model to explain these results in terms of a relatively stable negative regulatory factor.