Horwitz D A, Gray J D, Behrendsen S C, Kubin M, Rengaraju M, Ohtsuka K, Trinchieri G
University of Southern California School of Medicine, Los Angeles 90033, USA.
Arthritis Rheum. 1998 May;41(5):838-44. doi: 10.1002/1529-0131(199805)41:5<838::AID-ART10>3.0.CO;2-S.
To determine the profile of Th1-type and Th2-type cytokines produced by mononuclear cells from patients with recent-onset systemic lupus erythematosus (SLE), prior to the initiation of treatment with corticosteroids.
Using sensitive radioimmunoassays, interleukin-4 (IL-4), IL-10, IL-12 p40, tumor necrosis factor alpha (TNF alpha), interferon-gamma (IFN gamma), and granulocyte-macrophage colony-stimulating factor (GM-CSF) released into the culture supernatants of various unstimulated and stimulated blood mononuclear cell populations from 10 SLE patients was assessed in comparison with 10 matched healthy controls studied in parallel.
In early SLE, monocyte-enriched cells constitutively produced increased amounts of IL-10 and decreased amounts of IL-12 following stimulation. Lymphocyte-enriched cells in SLE produced decreased amounts of IFN gamma and TNF alpha following stimulation. In "rested" cells, these defects were accentuated and a defect in IL-12 production was suggested. Depletion studies suggested that CD8+ cells were a major source of TNF alpha and IFN gamma in controls, but not in SLE patients. Increased IL-4 production or abnormalities in GM-CSF production were not observed.
This study suggests that even early in the course of SLE, monocyte production of IL-10 is increased and that of IL-12 is decreased. Decreased production of Th1-type cytokines in SLE may be secondary to this imbalance between IL-10 and IL-12. A contributory role of dysfunctional CD8+ cells is suggested.
确定近期发病的系统性红斑狼疮（SLE）患者在开始使用皮质类固醇治疗前，单核细胞产生的Th1型和Th2型细胞因子的情况。
使用灵敏的放射免疫分析法，对10例SLE患者不同未刺激和刺激的血液单核细胞群体培养上清液中释放的白细胞介素-4（IL-4）、IL-10、IL-12 p40、肿瘤坏死因子α（TNFα）、干扰素-γ（IFNγ）和粒细胞-巨噬细胞集落刺激因子（GM-CSF）进行评估，并与10例平行研究的匹配健康对照进行比较。
在早期SLE中，富含单核细胞的细胞在刺激后组成性地产生增加量的IL-10和减少量的IL-12。SLE中富含淋巴细胞的细胞在刺激后产生减少量的IFNγ和TNFα。在“静止”细胞中，这些缺陷更加明显，并提示IL-12产生存在缺陷。去除研究表明，CD8 +细胞是对照组中TNFα和IFNγ的主要来源，但在SLE患者中不是。未观察到IL-4产生增加或GM-CSF产生异常。
本研究表明，即使在SLE病程早期，单核细胞产生的IL-10增加而IL-12减少。SLE中Th1型细胞因子产生减少可能继发于IL-10和IL-12之间的这种失衡。提示功能失调的CD8 +细胞起一定作用。
