Tsai Chang-Youh, Wu Tsai-Hung, Yu Chia-Li, Tsai Ying-Yang, Chou Chung-Tei
Section of Allergy, Immunology & Rheumatology, Department of Medicine, Taipei Veterans General Hospital, National Yang-Ming University, Taipei, Taiwan.
Immunol Invest. 2002 Aug-Nov;31(3-4):177-89. doi: 10.1081/imm-120016239.
Polymorphonuclear leukocytes (PMN) play an important role in eradicating bacterial infections. To test if PMN of patients with systemic lupus erythematosus (SLE) have defective capacity to produce IL-12, IL-12 p35 gene transcription and p70 excretion by PMN were evaluated in SLE patients and normal subjects. Peripheral blood PMN from 25 patients with active SLE and 25 normal individuals were stimulated with lipopolysaccharide (LPS, 100ng/mL) in the presence or absence of recombinant interferon (IFN)-gamma (5-200IU/mL). The IL-12 p35 gene transcripts were analyzed by reverse transcription - polymerase chain reaction (RT-PCR) and the IL-12 p70 in culture supenatants was quantified by enzyme immunoassay (EIA). At the 6th hour of stimulation, IL-12 expression in PMN of SLE patients was less prominent than that of the normal controls. The IL-12 was produced by normal PMN on LPS stimulation in the absence of IFN-gamma. IFN-gamma enhanced the IL-12 production by normal PMN stimulated with LPS, but it inhibited the IL-12 production in PMN from active lupus patients in the presence of LPS. Analysis with PCR using the same primers on the chromosomal DNA showed that p35 gene was intact in SLE patients. These results have suggested that SLE-PMN may have defect in IL-12 expression and the defect may be exaggerated in the presence of IFN-gamma which normally stimulates IL-12 production. This may account for increased susceptibility to multiple infections in patients with active SLE.
多形核白细胞（PMN）在根除细菌感染中发挥着重要作用。为了检测系统性红斑狼疮（SLE）患者的PMN产生白细胞介素-12（IL-12）的能力是否存在缺陷，对SLE患者和正常受试者的PMN的IL-12 p35基因转录和p70分泌进行了评估。在存在或不存在重组干扰素（IFN）-γ（5 - 200IU/mL）的情况下，用脂多糖（LPS，100ng/mL）刺激25例活动期SLE患者和25名正常个体的外周血PMN。通过逆转录 - 聚合酶链反应（RT-PCR）分析IL-12 p35基因转录本，并通过酶免疫测定（EIA）对培养上清液中的IL-12 p70进行定量。在刺激的第6小时，SLE患者PMN中的IL-12表达不如正常对照明显。在不存在IFN-γ的情况下，正常PMN在LPS刺激下产生IL-12。IFN-γ增强了LPS刺激的正常PMN的IL-12产生，但在存在LPS的情况下抑制了活动期狼疮患者PMN中的IL-12产生。使用相同引物对染色体DNA进行PCR分析表明，SLE患者的p35基因是完整的。这些结果表明，SLE-PMN可能在IL-12表达方面存在缺陷，并且在通常刺激IL-12产生的IFN-γ存在的情况下，该缺陷可能会被放大。这可能解释了活动期SLE患者对多种感染易感性增加的原因。
