Platelet C4d is highly specific for systemic lupus erythematosus

OBJECTIVE: Complement-activation product C4d is deposited on normal erythrocytes, while abnormal levels have been observed on the surface of erythrocytes of patients with systemic lupus erythematosus (SLE). This study examines whether C4d also deposits on human platelet surfaces, and whether platelet-bound C4d may provide a biomarker for SLE. METHODS: We conducted a cross-sectional study of 105 patients with SLE, 115 patients with other diseases, and 100 healthy controls. Levels of C4d on the surface of platelets were examined by flow cytometry and scanning confocal microscopy. Statistical analyses were performed to determine the clinical variables associated with platelet C4d. RESULTS: Abnormal levels of platelet C4d were found to be highly specific for SLE. Platelet C4d was detected in 18% of patients with SLE, being 100% specific for a diagnosis of SLE compared with healthy controls and 98% specific for SLE compared with patients with other diseases (P < 0.0001). In addition, platelet C4d was significantly associated with positivity for lupus anticoagulant (P < 0.0001) and anticardiolipin antibodies of the IgG (P = 0.035) or the IgM (P = 0.016) isotype. Platelet C4d was also significantly associated with SLE disease activity according to the SLE Disease Activity Index (P = 0.039), low serum C4 (P = 0.046), an elevated erythrocyte sedimentation rate (P = 0.006), and abnormal levels of C4d on erythrocytes (P < 0.0001). CONCLUSION: This observation suggests that platelet-bound C4d may be a useful biomarker for SLE and may be a clue to the pathogenic mechanisms responsible for the myriad thrombotic and vascular complications of lupus associated with antiphospholipid antibodies.     

Reticulocytes bearing C4d as biomarkers of disease activity for systemic lupus erythematosus

OBJECTIVE: There is an urgent need for biomarkers with which to monitor disease activity in patients with systemic lupus erythematosus (SLE). We recently showed that abnormal levels of C4d, an activation-derived fragment of complement component C4, are deposited on the surface of erythrocytes from patients with SLE. This study focused on reticulocytes, the youngest and shortest-lived erythrocytes (lifespan 24-48 hours), with the objective of testing our hypothesis that when reticulocytes emerge from the bone marrow, they are immediately exposed to and acquire C4d at levels proportionate to the extent of complement activation at that time, thereby reflecting disease activity in SLE. METHODS: We conducted a cross-sectional study of 156 patients with SLE, 140 patients with other diseases, and 159 healthy controls. Levels of C4d on the surface of reticulocytes were examined using a 2-color flow cytometric assay. The results were analyzed for correlations with SLE disease activity. RESULTS: A wide range of increased levels of reticulocyte C4d was specifically detected in SLE patients. These levels fluctuated in SLE patients and correlated with clinical disease activity, as determined by the Safety of Estrogens in Lupus Erythematosus: National Assessment (SELENA) version of the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) and the Systemic Lupus Activity Measure (SLAM). Specifically, in cross-sectional analyses, patients with reticulocyte C4d levels in the highest quartile compared with those in the lowest quartile had significantly higher SELENA-SLEDAI (P = 0.00002) and SLAM (P = 0.02) scores. Longitudinal observation demonstrated that the reticulocyte C4d levels changed in relation to the clinical course in individual patients. CONCLUSION: These findings support our hypothesis that C4d-bearing reticulocytes may serve as biomarkers of disease activity in patients with SLE.     

Low number of complement C3b/C4b receptors (CR1) on erythrocytes from patients with essential mixed cryoglobulinemia, systemic lupus erythematosus and rheumatoid arthritis: relationship with disease activity, anticardiolipin antibodies, complement activation and therapy.

Our aim was to assess whether the amount of complement C3b/C4b receptors (CR1) on erythrocytes shows a correlation to disease activity in various connective tissue diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and essential mixed cryoglobulinemia (EMC). Using an anti-CR1 monoclonal antibody, 26 patients with SLE, 34 with RA and 22 patients with EMC were investigated for erythrocyte CR1 expression. The control group consisted of 30 healthy individuals. The mean number of CR1/erythrocyte in the control group was 568 +/- 197 (range 174-1060), significantly higher than studied (EMC:379 +/- 248; p = 0.0005;SLE 147 +/- 56, p less than 0.0001; RA 298 +/- 177, p less than 0.0001). In patients with RA and in SLE, but not in patients with EMC, the number of CR1 numbers and anticardiolipin antibody (aCl) titers (r2 = 0.493; p = 0.034). A statistically significant correlation between CR1 numbers and CH50 values was found in patients with SLE, while in 3 patients with RA 4 months of therapy with cyclosporine A led to a further 30% reduction in CR1 number. Our conclusions are that (a) the decreased expression of erythrocyte CR1 is apparently a common feature of patients with various connective tissue diseases; (b) several acquired factors such as disease activity, complement activation, aCl and drugs may contribute to the loss of CR1 from erythrocytes; (c) in patients with RA and SLE, but not in patients with EMC, CR1 enumeration on erythrocytes may serve as a variable for clinical monitoring.     

Reduced numbers of complement receptor type 1 on erythrocytes are associated with increased levels of anticardiolipin antibodies. Findings in patients with systemic lupus erythematosus and the antiphospholipid syndrome

In several diseases, including systemic lupus erythematosus (SLE) and autoimmune hemolytic anemias, the numbers of complement receptor type 1 (CR1) expressed on erythrocytes of patients are reduced. In patients with SLE, anticardiolipin antibodies (aCL) have been associated with positive results on direct antiglobulin tests. Because of these findings, we investigated whether the reduced expression of erythrocyte CR1 in 61 patients (53 with SLE and 8 with the antiphospholipid syndrome) might be associated with the presence of aCL. A negative correlation was observed between aCL levels and mean numbers of CR1 (rs = -0.43, P = 0.001), and a positive correlation was observed between aCL levels and the levels of erythrocyte C4d and C3d (rs = 0.33 and 0.41, P = 0.01 and 0.001, respectively), but no correlation of aCL levels with serum C4 levels was found. When the results were further analyzed according to the IgG or IgM class of aCL, levels of antibodies of both classes were negatively correlated with CR1 numbers, but only IgM aCL levels were correlated with erythrocyte C4d and C3d numbers. The levels of anti-double-stranded DNA antibodies showed no correlation with erythrocyte CR1, C4d, or C3d numbers but were negatively correlated with serum C4 levels (rs = -0.43, P = 0.002). These data suggest that aCL, or a closely related antibody specificity, may bind to erythrocytes and may be directly involved in the mechanism for reduction of erythrocyte CR1 expression in SLE patients.     

Erythrocyte complement receptor type 1 in patients with systemic lupus erythematosus

Erythrocyte complement receptor type 1 (CR1) was measured in 71 patients with systemic lupus erythematosus (SLE) and 43 healthy controls. The level of erythrocyte CR1 in patients with SLE was significantly lower than that of controls and correlated with the disease activity of SLE. The more active the disease, the greater the decrease in erythrocyte CR1. The level of erythrocyte CR1 was inversely correlated with the level of circulating immune complexes (CIC) and was positively correlated with C3, CH50, factor B, and factor H. We also found lupus nephritis more frequently in patients with decreased erythrocyte CR1 than in those with normal levels of erythrocyte CR1. Our results suggest that the deficiency of erythrocyte CR1 in patients with SLE is acquired and may serve as a variable of clinical disease activity and may play a role in the pathogenesis of SLE.     

Measurement of cell‐bound complement activation products enhances diagnostic performance in systemic lupus erythematosus

Objective

To determine the value of cell‐bound complement activation products in combination with antinuclear antibody (ANA), anti–double‐stranded DNA antibody (anti‐dsDNA), and anti–mutated citrullinated vimentin antibody (anti‐MCV) for the diagnosis of systemic lupus erythematosus (SLE).

Methods

This was a multicenter cross‐sectional study in which 593 subjects were enrolled (210 SLE patients, 178 patients with other rheumatic diseases, and 205 healthy subjects). Complement receptor 1 levels on erythrocytes (ECR1) together with complement C4d levels on erythrocytes (EC4d), platelets (PC4d), and B cells (BC4d) were determined using fluorescence‐activated cell sorting. Serologic markers were measured by enzyme‐linked immunosorbent assay. Statistical analyses were performed using area under the curve (AUC), logistic regression, and calculations of diagnostic sensitivity and specificity.

Results

Anti‐dsDNA was an insensitive (30%) but specific (>95%) marker for SLE. Levels of EC4d, BC4d, and PC4d were several times higher, and levels of ECR1 lower, in SLE patients compared to patients with other rheumatic diseases and healthy subjects. Among 523 anti‐dsDNA–negative subjects, multivariate logistic regression analysis revealed that SLE was associated with ANA positivity (≥20 units), anti‐MCV negativity (≤70 units), and elevated levels of both EC4d and BC4d (AUC 0.918, P < 0.001). A positive index score corresponding to the weighted sum of these 4 markers correctly categorized 72% of SLE patients. Specificity in relation to patients with other rheumatic diseases and healthy controls was >90%. The combination of anti‐dsDNA and index score positivity yielded 80% sensitivity for SLE and 87% specificity against other rheumatic diseases.

Conclusion

An assay panel combining anti‐dsDNA, ANA, anti‐MCV, EC4d, and BC4d is sensitive and specific for the diagnosis of SLE.

     

Complement degradation product C3d in urine: marker of lupus nephritis

OBJECTIVE: To examine whether serum and urine C3d, a degradation product of C3, correlate with renal and extrarenal lupus activity. METHODS: Serum and urinary C3d levels were measured by ELISA in 15 healthy individuals and 24 patients with systemic lupus erythematosus (SLE) (8 with inactive disease, 7 with active but nonrenal disease, 9 with active lupus nephritis). Disease activity variables like serum C3, C4, and anti-dsDNA antibodies were also measured. RESULTS: The median serum C3d levels were significantly higher (p < 0.01) in patients with active (26 arbitrary units/ml; AU/ml) and inactive SLE (27 AU/ml) compared to healthy controls (11.25 AU/ml); levels were comparable in patients with active renal and extrarenal SLE. On the other hand, urine C3d was elevated only in patients with active SLE; its level was highest in patients with active lupus nephritis (0.87 AU/ml) compared to patients with active extrarenal diseases (0.31 AU/ml; p < 0.05), to patients with inactive lupus nephritis (0.06 AU/ml; p < 0.001), or to levels in healthy individuals (0.06; p < 0.001). Urine C3d showed stronger correlation with disease activity score (SLE Disease Activity Index) than serum C3, C4, anti-dsDNA antibodies, and serum C3d. CONCLUSION: Urine C3d is a good index of active lupus, particularly lupus nephritis.     

Prospective assessment of C4d deposits on circulating cells and renal tissues in lupus nephritis: a pilot study

Complement activation plays a key role in the pathogenesis of lupus nephritis (LN), a severe complication of systemic lupus erythematosus (SLE). We prospectively evaluated 15 LN subjects and two control groups: 13 non-SLE renal subjects (control A) and 239 SLE subjects without LN (control B). All had C4d levels on circulating erythrocytes (E-C4d), reticulocytes (R-C4d) and platelets (P-C4d) measured by flow cytometry, while C4d deposition in renal tissue was semiquantitatively assessed in LN subjects and control A using immunoperoxidase staining. Compared with control A, LN biopsies had higher glomerular-C4d scores (p?=?0.003), which were associated with more frequent granular glomerular immunofluorescence staining and electron dense deposits (p?相似文献   

Expression of Fcgamma and complement receptors on peripheral blood monocytes in systemic lupus erythematosus and rheumatoid arthritis

OBJECTIVES: Fcagamma and complement receptors play an important role in the interaction between immune complexes (IC) and monocytes/macrophages. Recent work has demonstrated that their relative expression on these cells may be modified by cytokines, including TNF-alpha and IL-4. Furthermore, cytokines may alter the expression of adhesion molecules such as ICAM-1. However, little data exist on the in vivo expression of specific Fcgamma and complement receptors in systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA), two diseases in which IC are important in pathogenesis. METHODS: Venous blood was obtained from 30 patients with SLE, 25 with RA and 25 healthy controls. Monocyte phenotype was determined by flow cytometric analysis of whole blood samples, with selective gating using forward and side scatter signals. Surface expression of Fcgamma receptors RI (CD64), RII (CD32) and RIII (CD16), complement receptors CR1 (CD35) and CR3 (CD11b/CD18), and adhesion molecules ICAM-1 (CD54) and CD11a (LFA-1) was determined. The effects of disease activity and corticosteroid therapy on the expression of these molecules were also examined. RESULTS: The expression of FcgammaRII was reduced on monocytes from patients with SLE compared with healthy controls and patients with RA (P = 0.002). This did not correlate with disease activity using conventional indices [SLEDAI (SLE disease activity index), C3/C4 levels and anti-double-stranded DNA antibody titres], and was independent of prednisolone therapy. There was no significant difference in FcgammaRI or RIII expression on SLE monocytes compared with healthy controls. In contrast, the expression of FcgammaRIII was increased on RA monocytes (P = 0.01), this being highest in patients with active disease. The proportion of FcgammaRIII-positive monocytes was also increased in RA, and prednisolone therapy was associated with a lower proportion of FcgammaRIII-positive cells. An increase in CR3 expression was seen on RA monocytes (P = 0.002), whilst CR1 was increased on monocytes from patients with active SLE or active RA. ICAM-1 expression was reduced on monocytes from patients with SLE (P = 0.002), although high-dose prednisolone therapy was associated with the lowest level of surface ICAM-1 on monocytes. CONCLUSIONS: Peripheral blood monocytes from patients with SLE or RA display significantly altered phenotypes compared with those from healthy controls. The observed reduction in SLE of FcgammaRII may represent a mechanism by which monocytes are protected from IC-mediated activation. Prednisolone therapy and disease activity had little effect on phagocytic receptor expression. The observed changes may reflect the different cytokine profiles seen in SLE and RA.     

Erythrocyte CR1 (C3b/C4b receptor) levels and disease activity in patients with SLE

Fifty-four patients with systemic lupus erythematosus (SLE) were examined for (1) CR1 (C3b/C4b receptor) levels on erythrocytes by an enzyme-linked immunosorbent assay, (2) levels of circulating immune complexes (IC) by a polyethylene glycol precipitation complement consumption method, and (3) concentrations of C3d split products in plasma by intermediate gel rocket immunoelectrophoresis. A preponderance of low CR1 levels was found among patients with SLE (mean 40%, range 13-106) as compared with normal controls (mean 70%, range 24-130) (p less than 0.001). The concentrations of circulating IC were elevated in 38% of 58 samples. The concentrations of C3d were elevated in 72%, and were positively correlated with the levels of IC (tau = 0.28; p less than 0.005) and with disease activity as assessed by a modification of the UCH/Middlesex criteria. Negative correlations were seen between the CR1 numbers and disease activity (p = 0.01), concentrations of circulating IC (tau = -0.14; p less than 0.005), and C3d (tau = -0.21; p less than 0.005). The changes found in CR1 levels on repeated study were, however, relatively small (less than or equal to 27%; median 5), even during periods of changing disease activity.     

The expression of C3b receptors in the differentiation of discoid lupus erythematosus and systemic lupus erythematosus

We studied the expression of the C3b receptor, CR1, on erythrocytes (E-CR1) of patients who, in spite of having mild systemic symptoms, were diagnosed as having discoid lupus erythematosus and followed accordingly. We found that E-CR1 was markedly reduced in these patients, similar to that seen in patients with systemic disease. In contrast, those patients with completely asymptomatic discoid lupus erythematosus had the same expression of E-CR1 as the normal population.     

Reduced uptake of apoptotic cells by macrophages in systemic lupus erythematosus: correlates with decreased serum levels of complement

BACKGROUND: Defects in phagocytosis of apoptotic cells have a role in the pathogenesis of autoimmune diseases. Decrease of phagocytosis of apoptotic cells occurs in systemic lupus erythematosus (SLE). Factors underlying this decrease are, presently, unknown. OBJECTIVE: To analyse the expression of relevant membrane receptors of monocyte derived macrophages (MDM) from patients with SLE and assess their ability to phagocytose apoptotic cells in comparison with MDM from healthy controls. Additionally, to compare phagocytosis in the presence of SLE sera with that in normal human serum (NHS). METHODS: Human peripheral blood monocytes were isolated from patients and controls, and cultured for 7 days to obtain MDM. Membrane expression of CD14, CD18, CD36, and CD51/61 was measured. MDM were incubated with apoptotic Jurkat cells in the presence of NHS or serum from patients with active or inactive disease. RESULTS: No differences in phagocytosis capacity were found between MDM from patients and controls. Membrane expression of the respective receptors was comparable in patients and controls. However, when MDM from controls were incubated with apoptotic cells in patient serum, phagocytosis was significantly decreased in comparison with incubation in NHS. This effect depended on the patients' disease activity and could be reversed by addition of NHS. Reduced uptake of apoptotic cells was associated with decreased levels of complement C1q, C4, and C3, but not with levels of complement factor B. CONCLUSIONS: Reduced uptake of apoptotic cells by MDM from patients with SLE is not an intrinsic defect but is serum dependent and associated with decreased levels of C1q, C4, and C3.     

Serum C4 levels in patients with systemic lupus erythematosus in remission

 Twenty-six patients with systemic lupus erythematosus (SLE) showing systemic lupus activity measure (SLAM) and SLE disease activity index (SLEDAI) scores ⩽2, as well as a lower C4 concentration than the mean C4 levels of healthy controls, were selected to evaluate the C4 levels of SLE patients in remission. Serum complement (CH50), complement components (C4, C3, and B), complement split products (C4d, iC3b, and Bb), phenotypic expression of C4 allotype, C4 production by peripheral blood monocytes, peripheral blood lymphocyte subpopulation, and interferon-gamma (IFN-γ) production were examined. In patients with SLE in remission, the C4 consumption (C4d/C4) was found to increase, and this was considered to be the most important factor for determining the serum concentration of C4. However, the relevance of the C4 allotypic expression was minimal. The IFN-γ-stimulated production of C4 by peripheral blood monocytes in SLE patients in remission was also less than that of the healthy controls. The IFN-γ-stimulated production of C4 in SLE patients in remission correlated with the peripheral blood CD4-positive cells. Less IFN-γ was produced by lymphocytes of SLE in remission than by those of healthy adults. We conclude that the serum C4 levels in SLE patients in remission reflect the degree of C4 consumption as well as the disease state, rather than genetic influences such as a C4A defect. Received: September 3, 2001 / Accepted: January 7, 2002 Present address: Center for Rheumatology and Rehabilitation, Beppu National Hospital, 1473 Uchikamado, Beppu 874-0011, Japan Tel. +81-977-67-1111; Fax +81-977-67-5766 e-mail: yasudamk@beppu.hosp.go.jp Correspondence to: M. Yasuda     

Distribution of the HindIII restriction fragment length polymorphism among patients with systemic lupus erythematosus with different concentrations of CR1.

Sixty six patients with systemic lupus erythematosus (SLE) were genotyped using a HindIII restriction fragment length polymorphism identified by CR1.1 cDNA, then were followed up for an average of 50 months to evaluate the stability of their CR1 activities. The gene frequencies for the two alleles which correlate with the numeric expression of CR1 on the erythrocytes were not significantly different between 66 patients with SLE and 52 normal controls. A discrepancy between homozygosity for a high allele and a negative CR1 activity was found in many patients. These patients, however, had significantly lower concentrations of serum complement than did patients with a positive CR1, and some were in an active state of the disease. Furthermore, there were several patients in whom the CR1 activities changed from negative to positive together with an increase in serum complement. Our results suggest that the decreased expression of CR1 on erythrocytes in patients with SLE is not inherited, rather it is a consequence of the disease processes.     

末端补体SC5b-9抗C1q抗体及补体C3 C4在狼疮疾病活动性判定中的价值

目的 探讨末端补体SC5b-9、抗C1q抗体及补体C3和C4在狼疮疾病活动性判定中的价值.方法 采用酶联免疫吸附试验(ELISA)检测系统性红斑狼疮(SLE)组62例、疾病对照组35例和健康对照组35名血清中的末端补体SC5b-9和抗C1q抗体水平,并检测血清中补体C3和C4的水平,并与SLE患者临床表现、病情活动度及狼疮肾炎(LN)的病理分型进行相关性分析.结果 在SLE活动组中末端补体SC5b-9和抗C1q抗体水平均显著高于各对照组(均P<0.05).末端补体SC5b-9和抗C1q抗体与补体C3、C4呈负相关(P<0.05),与SLE疾病活动指数(SLEDAI)呈正相关(P<0.05).联合检测对疾病活动的判断的敏感性和特异性分别为95%和98%.末端补体SC5b-9及抗C1q抗体在狼疮增殖件肾炎中表达明显高于膜性肾炎(均P<0.05).结论 联合检测可提高疾病诊断和活动性判断的特异性和敏感性;末端补体SC5b-9和抗C1q抗体参与了狼疮增殖性肾炎的免疫发病机制.     

末端补体SC5b-9抗C1q抗体及补体C3 C4在狼疮疾病活动性判定中的价值

目的 探讨末端补体SC5b-9、抗C1q抗体及补体C3和C4在狼疮疾病活动性判定中的价值.方法 采用酶联免疫吸附试验(ELISA)检测系统性红斑狼疮(SLE)组62例、疾病对照组35例和健康对照组35名血清中的末端补体SC5b-9和抗C1q抗体水平,并检测血清中补体C3和C4的水平,并与SLE患者临床表现、病情活动度及狼疮肾炎(LN)的病理分型进行相关性分析.结果 在SLE活动组中末端补体SC5b-9和抗C1q抗体水平均显著高于各对照组(均P<0.05).末端补体SC5b-9和抗C1q抗体与补体C3、C4呈负相关(P<0.05),与SLE疾病活动指数(SLEDAI)呈正相关(P<0.05).联合检测对疾病活动的判断的敏感性和特异性分别为95%和98%.末端补体SC5b-9及抗C1q抗体在狼疮增殖件肾炎中表达明显高于膜性肾炎(均P<0.05).结论 联合检测可提高疾病诊断和活动性判断的特异性和敏感性;末端补体SC5b-9和抗C1q抗体参与了狼疮增殖性肾炎的免疫发病机制.     

末端补体SC5b-9抗C1q抗体及补体C3 C4在狼疮疾病活动性判定中的价值

目的 探讨末端补体SC5b-9、抗C1q抗体及补体C3和C4在狼疮疾病活动性判定中的价值.方法 采用酶联免疫吸附试验(ELISA)检测系统性红斑狼疮(SLE)组62例、疾病对照组35例和健康对照组35名血清中的末端补体SC5b-9和抗C1q抗体水平,并检测血清中补体C3和C4的水平,并与SLE患者临床表现、病情活动度及狼疮肾炎(LN)的病理分型进行相关性分析.结果 在SLE活动组中末端补体SC5b-9和抗C1q抗体水平均显著高于各对照组(均P<0.05).末端补体SC5b-9和抗C1q抗体与补体C3、C4呈负相关(P<0.05),与SLE疾病活动指数(SLEDAI)呈正相关(P<0.05).联合检测对疾病活动的判断的敏感性和特异性分别为95%和98%.末端补体SC5b-9及抗C1q抗体在狼疮增殖件肾炎中表达明显高于膜性肾炎(均P<0.05).结论 联合检测可提高疾病诊断和活动性判断的特异性和敏感性;末端补体SC5b-9和抗C1q抗体参与了狼疮增殖性肾炎的免疫发病机制.     

末端补体SC5b-9抗C1q抗体及补体C3 C4在狼疮疾病活动性判定中的价值

目的 探讨末端补体SC5b-9、抗C1q抗体及补体C3和C4在狼疮疾病活动性判定中的价值.方法 采用酶联免疫吸附试验(ELISA)检测系统性红斑狼疮(SLE)组62例、疾病对照组35例和健康对照组35名血清中的末端补体SC5b-9和抗C1q抗体水平,并检测血清中补体C3和C4的水平,并与SLE患者临床表现、病情活动度及狼疮肾炎(LN)的病理分型进行相关性分析.结果 在SLE活动组中末端补体SC5b-9和抗C1q抗体水平均显著高于各对照组(均P<0.05).末端补体SC5b-9和抗C1q抗体与补体C3、C4呈负相关(P<0.05),与SLE疾病活动指数(SLEDAI)呈正相关(P<0.05).联合检测对疾病活动的判断的敏感性和特异性分别为95%和98%.末端补体SC5b-9及抗C1q抗体在狼疮增殖件肾炎中表达明显高于膜性肾炎(均P<0.05).结论 联合检测可提高疾病诊断和活动性判断的特异性和敏感性;末端补体SC5b-9和抗C1q抗体参与了狼疮增殖性肾炎的免疫发病机制.     

Complement activation in systemic lupus erythematosus: a marker of inflammation

Previous investigators have established that complement activation occurs in patients with systemic lupus erythematosus (SLE). Utilizing a new rapid method, an ELISA for C3d as a measure of activation products, 83 SLE plasmas and 24 controls were assayed. A retrospective correlation of C3d levels with the clinical assessment defined 4 subgroups of SLE patients: Group 1--clinically well with normal C3d levels (25%), Group 2--clinically ill with elevated C3d levels (34%), Group 3--clinically well with elevated C3d levels (39%), the largest group, and Group IV--clinically ill with normal C3d levels (2%). In the group of overtly ill patients with elevated C3d levels (Group 2) who were studied serially, C3d levels correlated with disease activity, suggesting that elevated C3d levels may be a marker for active SLE. Further prospective study is required to determine the significance of elevated C3d levels in clinically well patients.