Toubi E, Adir-Shani A, Kessel A, Shmuel Z, Sabo E, Hacham H
Division of Clinical Immunology and Allergy, Bnai Zion Medical Center, Haifa, Israel.
J Clin Immunol. 2000 Sep;20(5):371-8. doi: 10.1023/a:1006624331022.
To investigate the pathophysiology of chronic urticaria (CU) in light of the abundant evidences that it is an autoimmune disease and to define some cellular markers in B/T lymphocytes that could be of pathogenic significance, we investigated 14 patients suffering from CU, compared to 7 contact dermatitis patients and 10 normal control individuals. We tested the expression of CD5, B7.1 (CD80), CD23, and CD25 on B cells and of CD(40L)) and CD25 on T cells from all studied individuals. We also tested B cell proliferation upon their activation followed by dexamethazone induced inhibition of proliferation. The expression of bcl-2 protein in activated lymphocytes from normal individuals was compared to that of contact dermatitis and CU patients. CD(40L) expression was found significantly higher on in (vitro activated CD3 [with phorbol myristate acetate (PMA) and ionomycine Ca2+ at 12 hr of culture] from CU patients compared to that of contact dermatitis and normal individuals. Whereas the proliferation of activated B cells from CU patients was higher, dexamethazone-induced inhibition of B cell proliferation was found statistically similar in both groups yet lower in B cells from most severe CU patients. We demonstrate a higher bcl-2 expression in activated B and T lymphocytes of severe CU patients compared to that of moderate CU and both contact dermatitis and normal individuals. The increased expression of CD(40L) on activated T cells might play a role in the polyclonal increased B cell proliferation of CU patients. This increased proliferation accompanies the finding that activated B and T lymphocytes from these patients demonstrate increased bcl-2 expression. The resistance of some B cells to dexamethazone-induced inhibition of proliferation encourages us to investigate the possibility that B cells from some CU patients might develop rescue mechanisms from activated cell death. These findings provide further evidence that CU is indeed an autoimmune disease, although its precise nature has yet to be fully elucidated.
鉴于有大量证据表明慢性荨麻疹（CU）是一种自身免疫性疾病，为了研究其病理生理学，并确定B/T淋巴细胞中一些可能具有致病意义的细胞标志物，我们对14例CU患者进行了研究，并与7例接触性皮炎患者和10名正常对照个体进行了比较。我们检测了所有研究对象B细胞上CD5、B7.1（CD80）、CD23和CD25以及T细胞上CD(40L)和CD25的表达。我们还检测了B细胞激活后的增殖情况以及地塞米松诱导的增殖抑制。将正常个体激活淋巴细胞中bcl-2蛋白的表达与接触性皮炎和CU患者的进行比较。发现与接触性皮炎患者和正常个体相比，CU患者体外（用佛波酯肉豆蔻酸酯乙酸盐（PMA）和离子霉素Ca2+在培养12小时时）激活的CD3上CD(40L)的表达显著更高。虽然CU患者激活B细胞的增殖更高，但地塞米松诱导的B细胞增殖抑制在两组中在统计学上相似，不过在最严重的CU患者的B细胞中更低。我们证明，与中度CU患者以及接触性皮炎患者和正常个体相比，重度CU患者激活的B和T淋巴细胞中bcl-2表达更高。激活T细胞上CD(40L)表达的增加可能在CU患者B细胞多克隆增殖增加中起作用。这种增殖增加伴随着这些患者激活的B和T淋巴细胞中bcl-2表达增加的发现。一些B细胞对地塞米松诱导的增殖抑制具有抗性，这促使我们研究一些CU患者的B细胞可能从激活的细胞死亡中发展出挽救机制的可能性。这些发现提供了进一步的证据，表明CU确实是一种自身免疫性疾病，尽管其确切性质尚未完全阐明。
