Effect of LACK and KMP11 on IFN-γ production by peripheral blood mononuclear cells from cutaneous and mucosal leishmaniasis patients
Effect of LACK and KMP11 on IFN-γ production by peripheral blood mononuclear cells from cutaneous and mucosal leishmaniasis patients
复制标题
DOI：
10.1111/j.1365-3083.2005.01581.x
复制
发表时间：
2005-04-01
影响因子：
3.7
通讯作者：
de Jesus, AR
中科院分区：
文献类型：
--
作者：
Carvalho, LP;Passos, S;de Jesus, AR
观察重组抗原激动质粒膜蛋白11(KMP11)和活化C激酶受体同源物利什曼原虫(LACK)在皮肤利什曼病(CL)和粘膜利什曼病(ML)患者中的免疫调节作用。ML和CL患者外周血单个核细胞经SLA刺激后产生的干扰素-γ平均水平分别为5625+/-2333pg/ml和4422+/-3665pg/ml。在KMP11或LACK刺激的培养中未检测到干扰素-γ。IL-10浓度分别为13+/-12pg/ml、285+/-388pg/ml和802+/-483pg/ml。在CL和ML患者经SLA刺激的PBMC中加入KMP11或缺乏KMP11可增加IL-10的产生(P<；0.05)。加入KMP11可使CL患者和ML患者的干扰素-γ水平分别降低52%和19%。在SLA刺激的培养中加入LACK，可使CL患者和ML患者的干扰素-γ水平分别降低58%和30%。IL-10的中和取消了LACK和KMP11的下调作用。LACK和KMP11的调节作用是由于诱导IL-10的产生，可能有助于减轻慢性炎症性疾病。然而，在某些临床情况下，就像ML所证明的那样，这些分子不能抑制干扰素-伽马反应，甚至不能诱导IL-10的产生。
The immune modulatory properties of recombinant antigens Kinetoplasmid membrane protein-11 (KMP11) and Leishmania homologue of receptors for activated C kinase (LACK) in cutaneous leishmaniasis (CL) and mucosal leishmaniasis (ML) patients were evaluated. The mean levels of interferon-gamma (IFN-gamma) in soluble leishmania antigen (SLA) stimulated peripheral blood mononuclear cells (PBMC) of ML and CL patients were 5625 +/- 2333 pg/ml and 4422 +/- 3665 pg/ml, respectively. IFN-gamma was not detected in Cultures stimulated with KMP11 or LACK. Interletikin-10 (IL-10) concentration in SLA, KMP1 I and LACK-stimulated PBMC of ML patients was 13 +/- 12 pg/ml, 285 +/- 388 pg/ml and 802 +/- 483 pg/ml, respectively. Addition of KMP11 or LACK to SLA-stimulated PBMC of CL and ML patients enhanced IL-10 production (P< 0.05). Addition of KMP11 decreased IFN-gamma levels by 52% in CL patients and by 19% in ML patients. Addition of LACK to SLA-stimulated cultures decreased IFN-gamma levels by 58% in CL patients and by 30% in ML patients. Neutralization of IL-10 abrogated the downregulatory effect of LACK and KMP11. The modulatory properties of LACK and KMP11 are due to induction of IL-10 production and may be helpful for attenuating chronic inflammatory diseases. However, in some clinical conditions, as demonstrated for ML, these molecules are not able to suppress the IFN-gamma response, even inducing IL-10 production.