Gattorno M, Vignola S, Barbano G, Sormani M P, Sabatini F, Buoncompagni A, Picco P, Pistoia V
2nd Division of Pediatrics, The G. Gaslini Scientific Institute for Children, Genoa, Italy.
J Rheumatol. 2000 Sep;27(9):2251-5.
Animal models of immune complex mediated tissue injury have shown that tumor necrosis factor (TNF) and TNF induced adhesion molecules play an important role in the pathogenesis of tissue damage mediated by IgG, but not in that mediated by IgA, immune complexes. We compared possible differences in the behavior of 2 TNF induced adhesion molecules (VCAM-1 and ICAM-1) in Henoch-Schönlein purpura (HSP), which is characterized by the formation of IgA immune complexes, versus systemic lupus erythematosus (SLE), which is mostly associated with the vascular deposition of IgG immune complexes.
Serum concentrations of soluble (s)VCAM-1 and ICAM-1 were determined by ELISA methods in 20 patients with pediatric SLE showing variably active disease, 20 active patients with active HSP, and 19 healthy controls. TNF-alpha as well as p55 and p75 soluble receptors (sTNF-R) were simultaneously tested by enzyme amplified sensitivity immunoassay in 22 patients (12 SLE, 10 HSP).
Serum sVCAM-1 concentration was significantly higher in patients with SLE (mean +/- SD, 608 +/- 76 ng/ml), than in patients with HSP (501.9 +/- 63.3 ng/ml) and controls (446.8 +/- 139.2 ng/ml) (p < 0.001). In SLE patients, sVCAM-1 correlated positively with ESR (r = 0.45, p = 0.02) and negatively with C4 serum levels (r = -0.57, p = 0.004), platelets (r = -0.38, p = 0.03), and lymphocyte count (r = -0.42, p = 0.03). No differences in sICAM-1 serum concentrations were detected among SLE, HSP, or control groups. Soluble VCAM, but not sICAM-1, showed a positive correlation with TNF-alpha (r = 0.71, p = 0.01), p55 (r = 0.63, p = 0.02), and p75 (r = 0.7, p = 0.01) sTNF-R serum concentrations in SLE, but not in patients with HSP.
Our study provides additional evidence of a possible differential involvement of TNF and TNF induced adhesion molecules in the pathogenesis of tissue damage between pediatric SLE and HSP.
免疫复合物介导的组织损伤动物模型表明，肿瘤坏死因子（TNF）及TNF诱导的黏附分子在IgG介导的组织损伤发病机制中起重要作用，但在IgA免疫复合物介导的组织损伤中并非如此。我们比较了2种TNF诱导的黏附分子（血管细胞黏附分子-1（VCAM-1）和细胞间黏附分子-1（ICAM-1））在以IgA免疫复合物形成为特征的过敏性紫癜（HSP）与主要与IgG免疫复合物血管沉积相关的系统性红斑狼疮（SLE）中的行为可能存在的差异。
采用酶联免疫吸附测定（ELISA）法测定20例疾病活动程度各异的儿童SLE患者、20例活动期HSP患者及19名健康对照者血清中可溶性（s）VCAM-1和ICAM-1的浓度。采用酶放大敏感性免疫测定法同时检测22例患者（12例SLE、10例HSP）的肿瘤坏死因子-α（TNF-α）以及p55和p75可溶性受体（sTNF-R）。
SLE患者血清sVCAM-1浓度（均值±标准差，608±76 ng/ml）显著高于HSP患者（501.9±63.3 ng/ml）和对照者（446.8±139.2 ng/ml）（p<0.001）。在SLE患者中，sVCAM-1与红细胞沉降率（ESR）呈正相关（r=0.45，p=0.02），与血清C4水平呈负相关（r=-0.57，p=0.004），与血小板（r=-0.38，p=0.03）及淋巴细胞计数（r=-0.42，p=0.03）呈负相关。SLE组、HSP组及对照组之间未检测到sICAM-1血清浓度存在差异。可溶性VCAM而非sICAM-1在SLE患者中与TNF-α（r=0.71，p=0.01）、p55（r=0.63，p=0.02）及p75（r=0.7，p=0.01）的sTNF-R血清浓度呈正相关，但在HSP患者中并非如此。
我们的研究为TNF及TNF诱导的黏附分子在儿童SLE和HSP组织损伤发病机制中可能存在的不同参与情况提供了更多证据。
