Babaloo Z, Kaye P M, Eslami M B
Tabris University of Medical Sciences, Department of Immunology, Tabriz, Iran.
Trans R Soc Trop Med Hyg. 2001 Jan-Feb;95(1):85-8. doi: 10.1016/s0035-9203(01)90344-x.
The role of interleukin (IL)-13, a Th2 cytokine sharing many of the features of IL-4, has not previously been examined in patients with visceral leishmaniasis (VL). We examined sera from Iranian patients with VL caused by Leishmania infantum. Serum IL-13 was detected in 50% (22/44) of patients with active primary disease. In comparison, IL-10 was detected in 79.5% (35/44), interferon gamma (IFN gamma) in 38.5% (17/44), and IL-4 in only 5% (2/44) of these patients. With few exceptions all 3 cytokines were undetectable after clinical recovery following antimony therapy. Five of 7 patients (71%) who failed antimony therapy and had relapsing disease had similar levels of IL-10 to patients with active primary disease. However, with only 1 exception, IL-13, IFN gamma and IL-4 were not detected in such patients. These data suggest that relapsing disease may result from defective cellular immunity, unrelated to immunosuppression mediated by IL-10.
白细胞介素（IL）-13是一种具有许多IL-4特征的Th2细胞因子，此前尚未在内脏利什曼病（VL）患者中进行过研究。我们检测了来自伊朗因婴儿利什曼原虫引起的VL患者的血清。在50%（22/44）的活动性原发性疾病患者中检测到血清IL-13。相比之下，在这些患者中，79.5%（35/44）检测到IL-10，38.5%（17/44）检测到干扰素γ（IFNγ），仅5%（2/44）检测到IL-4。除少数例外，在锑剂治疗后临床康复后，所有这三种细胞因子均检测不到。7例锑剂治疗失败且疾病复发的患者中有5例（71%）的IL-10水平与活动性原发性疾病患者相似。然而，除1例例外，在此类患者中未检测到IL-13、IFNγ和IL-4。这些数据表明，复发性疾病可能是由于细胞免疫缺陷所致，与IL-10介导的免疫抑制无关。
