Teague T K, Marrack P, Kappler J W, Vella A T
Department of Medicine, National Jewish Center for Immunology and Respiratory Medicine, Denver, CO 80206, USA.
J Immunol. 1997 Jun 15;158(12):5791-6.
It has previously been demonstrated that mature mouse T cells live for many weeks in vivo. In contrast, explanted lymph node or splenic T cells undergo spontaneous death within days, suggesting that survival factors supplied in vivo are not present in normal tissue culture medium. We discovered that IL-6 can rescue resting T cells from apoptosis in vitro. We show that recombinant mouse IL-6 as well as IL-6 in endothelial cell supernatants are sufficient to rescue T cells from death in the absence of additional cytokines. We show that CD4+ T cells express Bcl-2 immediately following isolation from the mouse, but after 24 h in culture Bcl-2 is undetectable. If during this time period the T cells are incubated with rIL-6, Bcl-2 expression is not down-regulated. It is, therefore, possible that IL-6 rescue from death is mediated by maintenance or induction of Bcl-2 expression. Addition of rIL-6 does not by itself induce blastogenesis or proliferation, and therefore, this cytokine appears to be a true survival factor rather than a mitogenic factor for resting T cells. Together, these results support a potential role for IL-6 as one of the factors important for prolonging resting T cell survival in vivo.
先前已经证明，成熟的小鼠T细胞在体内能存活数周。相比之下，体外培养的淋巴结或脾脏T细胞在数天内就会自发死亡，这表明体内提供的存活因子在正常组织培养基中并不存在。我们发现IL-6能够在体外挽救静息T细胞免于凋亡。我们表明，重组小鼠IL-6以及内皮细胞上清液中的IL-6足以在没有其他细胞因子的情况下挽救T细胞免于死亡。我们发现，CD4+ T细胞从小鼠分离后立即表达Bcl-2，但培养24小时后就检测不到Bcl-2了。如果在此时间段内将T细胞与rIL-6一起孵育，Bcl-2的表达就不会下调。因此，IL-6挽救细胞免于死亡可能是通过维持或诱导Bcl-2的表达来介导的。添加rIL-6本身并不会诱导细胞分裂或增殖，因此，这种细胞因子似乎是一种真正的存活因子，而不是静息T细胞的促有丝分裂因子。总之，这些结果支持IL-6作为延长体内静息T细胞存活的重要因子之一的潜在作用。
