Söderberg O, Christiansen I, Carlsson M, Nilsson K
Department of Pathology, University of Uppsala, University Hospital, Sweden.
Scand J Immunol. 1997 Jun;45(6):706-14. doi: 10.1046/j.1365-3083.1997.d01-451.x.
This paper reports on differences between B cell-type chronic lymphocytic leukaemia (B-CLL) and normal B cells in their response to IL-2+thioredoxin (Trx), Staphylococcus aureus Cowan strain 1 (SAC)+IL-2+Trx, and to CD40 ligation of IL-2+Trx and SAC+IL-2+Trx stimulation. The authors found that Trx acted synergistically with IL-2 and SAC+IL-2 in inducing DNA synthesis in B-CLL cells, but not in the normal B cells. Interestingly, IL-2+Trx alone was found to induce proliferation in B-CLL cells from patients with advanced stages of disease. In addition, we also found that IL-2+Trx and SAC+IL-2+Trx-induced DNA synthesis of B-CLL cells was inhibited by CD40 activation (by soluble anti-CD40 MoAb and anti-CD40 MoAb presented on irradiated CD32L cells). In clear contrast, SAC+IL-2+ Trx-induced DNA synthesis of normal B cells was not inhibited by soluble anti-CD40 MoAb. The authors therefore conclude that B-CLL cells differ from normal B cells in their response to IL-2 (IL-2+Trx) and CD40 ligation.
本文报道了B细胞型慢性淋巴细胞白血病（B-CLL）与正常B细胞在对白细胞介素-2+硫氧还蛋白（Trx）、金黄色葡萄球菌考恩1株（SAC）+白细胞介素-2+Trx以及白细胞介素-2+Trx和SAC+白细胞介素-2+Trx刺激下CD40连接反应方面的差异。作者发现，Trx与白细胞介素-2以及SAC+白细胞介素-2协同作用，诱导B-CLL细胞中的DNA合成，但对正常B细胞无此作用。有趣的是，单独的白细胞介素-2+Trx被发现可诱导疾病晚期患者的B-CLL细胞增殖。此外，我们还发现，CD40激活（通过可溶性抗CD40单克隆抗体和照射的CD32L细胞上呈现的抗CD40单克隆抗体）可抑制白细胞介素-2+Trx和SAC+白细胞介素-2+Trx诱导的B-CLL细胞DNA合成。与之形成鲜明对比的是，可溶性抗CD40单克隆抗体并未抑制SAC+白细胞介素-2+Trx诱导的正常B细胞DNA合成。因此，作者得出结论，B-CLL细胞在对白细胞介素-2（白细胞介素-2+Trx）和CD40连接的反应上与正常B细胞不同。
