Wrenshall L E, Platt J L
Department of Surgery, University of Washington, Seattle 98195, USA.
J Immunol. 1999 Oct 1;163(7):3793-800.
Although IL-2 is commonly thought to promote proliferation of T lymphocytes, mice deficient in IL-2 exhibit splenomegaly, lymphocytosis, and autoimmunity, suggesting this cytokine may have a prominent role in T cell homeostasis. Since the number of T cells in the bloodstream and lymphoid organs is tightly controlled, it is likely that the availability of IL-2 must also be closely regulated. One mechanism altering the local availability of cytokines is association with heparan sulfate, a glycosaminoglycan found on cell surfaces and within extracellular matrices. Here we show that an association between IL-2 and heparan sulfate localizes IL-2 to lymphoid organs such as the spleen. We also show that IL-2, sequestered in this way, contributes to the activation of T lymphocytes and primes T lymphocytes for activation-induced cell death.
尽管通常认为白细胞介素-2（IL-2）能促进T淋巴细胞增殖，但缺乏IL-2的小鼠表现出脾肿大、淋巴细胞增多和自身免疫，这表明这种细胞因子可能在T细胞稳态中起重要作用。由于血液和淋巴器官中T细胞的数量受到严格控制，IL-2的可用性也可能受到密切调节。改变细胞因子局部可用性的一种机制是与硫酸乙酰肝素结合，硫酸乙酰肝素是一种存在于细胞表面和细胞外基质中的糖胺聚糖。在这里，我们表明IL-2与硫酸乙酰肝素之间的结合将IL-2定位到脾脏等淋巴器官。我们还表明，以这种方式隔离的IL-2有助于T淋巴细胞的激活，并使T淋巴细胞为激活诱导的细胞死亡做好准备。
