B cell activation in clinically quiescent systemic lupus erythematosus (SLE) is related to immunoglobulin levels, but not to levels of anti-dsDNA, nor to concurrent T cell activation.

In clinically quiescent SLE hypergammaglobulinaemia, presence of autoantibodies, and increased soluble IL-2 receptors (sIL-2R) have been reported, suggesting persistent B as well as T cell activation. In contrast, the primary immune response to test antigens is markedly decreased. To analyse these phenomena at a cellular level, we undertook a cross-sectional study on 13 non-active SLE patients and 15 controls. We determined the composition of lymphocyte subsets with special attention to activation markers (CD25, HLA-DR, CD38) and the presence of naive T cells (CD45RO-), and related those findings to serological parameters. In non-active SLE patients the expression of activation markers on B cells and T cells was higher than in normal controls (P < or = 0.02), but was not interrelated. Percentages of activated B cells in SLE were related to levels of total IgG (P < 0.02) and IgM (P < 0.02) but not to anti-dsDNA, suggesting a disordered immune system also in clinically quiescent SLE. Numbers of CD4+ cells (P < 0.001) and CD4+CD45RO- cells (P < 0.05) were decreased. The latter finding might explain the anergy to primary test antigens in clinically quiescent SLE.     

Levels of soluble VCAM-1, soluble ICAM-1, and soluble E-selectin during disease exacerbations in patients with systemic lupus erythematosus (SLE); a long term prospective study.

Active SLE is characterized by immune deposits and subsequent vascular inflammation in many organs. Expression and up-regulation of adhesion molecules is basic to migration of inflammatory cells into the tissues. Recently, soluble isoforms of these molecules have been described which might be an expression of their up-regulation in the tissues and, as such, of disease activity. The purpose of this study was to evaluate whether changes in levels of soluble adhesion molecules reflect disease activity. We analysed serial sera in a 6-month period preceding 22 consecutive exacerbations of SLE for levels of soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), and sE-selectin. Levels were related to clinical disease activity (SLEDAI), and levels of anti-dsDNA and complement. At the time of maximal disease activity, levels of sVCAM-1 in patients with SLE were higher than those in controls (P < 0.0001), levels in patients with renal involvement being higher than in those without (P < 0.02). Levels of sVCAM-1 correlated with SLEDAI scores (P < 0.05) and, inversely, with levels of C3 (P = 0.01). In addition, in the presence of anti-dsDNA, levels of sVCAM-1 tended to correlate with levels of these autoantibodies (P < 0.1). Levels of sICAM-1 were normal and sE-selectin levels even decreased compared with controls. Levels of sVCAM-1 were higher at the moment of relapse (P = 0.001) than at 6 months before this time point. This rise correlated with the rise in SLEDAI score (P < 0.02). Levels of sICAM-1 and sE-selectin did not rise, and remained in the normal range in all exacerbations studied. In conclusion, in contrast to sICAM-1 and sE-selectin, levels of sVCAM-1 are increased, rise parallel to disease activity during exacerbations in SLE, and are associated with decreasing levels of complement factors. This favours the hypothesis of immune deposit formation, activation of the complement cascade and activation of endothelial cells. Concurrent up-regulation of vascular adhesion molecules may thus result in transmigration of activated inflammatory cells inducing tissue damage.     

HLA-DR expression on lymphocyte subsets as a marker of disease activity in patients with systemic lupus erythematosus

A major problem in the management of SLE patients is to predict a flare or to distinguish between active and quiescent disease. Serological markers are widely used to assess disease activity, but many patients have close to or normal values for these parameters while exhibiting obvious disease-related signs and symptoms. This study aimed to determine which serological parameters, among ESR, ANA and anti-dsDNA antibody titres, CH50 and the HLA-DR expression on circulating T-lymphocyte subsets, best reflected the development of SLE flares. Sixty SLE patients were included, 34 with quiescent disease throughout the entire follow-up period and 26 who experienced an SLE flare defined as having active disease. According to univariate analysis, all parameters were significantly higher for patients with active disease, with the percentage of CD8+DR+ cells being the most significant parameter (P = 10-7). Multivariate logistic regression analysis identified three independent variables enabling the identification of a lupus flare: CH50, the CD8+DR+ and CD4+DR+ cell percentages among total lymphocytes. The CD8+DR+ cell percentage is the biological parameter most significantly associated with a flare (P < 0.001), even more powerful than CH50 (P < 0.01). HLA-DR expression on CD8+ lymphocytes clearly coincided with disease evolution in seven patients enrolled as having quiescent disease, but who experienced one flare during follow-up that subsequently resolved. The percentage of circulating CD8+DR+ lymphocytes appears to be a biological marker which accurately reflects disease activity. A larger prospective study is needed to demonstrate the real efficacy of this marker in predicting an exacerbation in SLE patients.     

Bronchoalveolar lavage cell analysis and lung function impairment in patients with systemic lupus erythematosus (SLE).

We examined the relationship between peripheral blood and bronchoalveolar lavage (BAL) lymphocyte phenotypes and lung function in 19 patients with SLE, and evaluated their association with disease activity. Lung function assessment showed a mildly restrictive pattern with frequent impairment of transfer factor for carbon monoxide (T1,co) and diffusing capacity of the alveolocapillary membrane (Dm), of late-expiratory airflow rates and with a high prevalence of increased airway resistance. T1,co, Kco and Dm correlated inversely with the numbers of CD8+ cells and CD56+/CD16+/CD3- (NK) cells in BAL. Oxygen radical production, both by stimulated and unstimulated BAL cells and blood polymorphonuclear leucocytes (PMN) was significantly increased in SLE. In comparison with healthy controls, patients with SLE had a lower percentage of CD19+ B cells in the BAL versus an increased percentage of these cells in peripheral blood. HLA-DR expression on CD4+ and CD8+ lung lymphocytes was markedly increased in SLE. Current SLE disease activity was not associated with changes in BAL or peripheral blood lymphocyte phenotypes. Our data suggest that an ongoing cell-mediated immune response is present in the lungs in SLE, particularly involving activated CD8+ T cells and CD56+/CD16+/CD3- NK cells. It is associated with up-regulated local production of oxygen radicals and with impaired pulmonary diffusing capacity. This inflammatory process seems to be independent of general SLE disease activity.     

Complement receptor 1 (CR1) on erythrocytes of patients with systemic lupus erythematosus

Ninety-five (85%) of the 112 Japanese patients with systemic lupus erythematosus (SLE) were negative for the complement receptor 1 (CR1) activities on erythrocytes, while 770 (91%) of the 847 normal subjects were positive for CR1, as determined by immune-adherence hemagglutination. Pedigree analyses of the normal population suggested that the phenotype of negative CR1 was determined by a autosomal recessive gene. Among 112 SLE patients, 73 (65%) showed persistently negative CR1 during remission for over 26 months of follow-up, although the CR1 levels did vary with the disease activity in 22 SLE patients. These results show that the relative risk for developing SLE in persons with negative CR1 is 19. CR1 activity appears to be an important genetic factor related the development of SLE.     

Heterogeneity of binding reactivity to different phospholipids of antibodies from patients with systemic lupus erythematosus (SLE) and with syphilis.

The binding specificities were investigated of anti-phospholipid antibodies derived from sera from 55 patients with SLE and related diseases, and from 33 patients with syphilis. Antibodies from both these groups of patients bind strongly to cardiolipin in solid-phase immunoassays, but only antiphospholipid antibodies from patients with autoimmune diseases are associated with thrombotic complications and recurrent spontaneous abortions. IgG anti-phospholipid antibodies from both groups of patients cross-reacted with a range of negatively charged phospholipids, but binding to neutral phospholipids was largely restricted to sera from patients with syphilis. A monoclonal IgM lambda anti-cardiolipin antibody, derived from a patient with autoimmunity, was used to inhibit binding of anti-phospholipid antibodies to cardiolipin and to phosphatidic acid. This antibody inhibited the binding of autoimmune sera to cardiolipin more strongly than sera from syphilis patients, but the converse pattern of inhibition of binding to phosphatidic acid was observed. The VDRL titre correlated with anti-phospholipid antibody activity in sera from syphilis patients, but not from those with autoimmunity. Lupus anti-coagulant activity correlated weakly with IgG antibody levels to each of the negatively charged phospholipids among the patients with autoimmunity. Lupus anticoagulant activity did not correlate uniquely with any anti-phospholipid antibody specificity. These results provide further documentation of the great heterogeneity of anti-phospholipid antibodies associated with autoimmune disease and syphilis.     

IL-18对系统性红斑狼疮患者淋巴细胞凋亡和P53蛋白表达的影响

目的　研究系统性红斑狼疮 (SLE)患者外周血淋巴细胞在体外IL 1 8刺激培养下细胞凋亡及P53蛋白表达情况。方法　AnnexinV联合PI染色定量法及免疫荧光染色法 ,分析了 44例SLE患者和 30例正常人外周淋巴细胞在体外IL 1 8刺激培养后凋亡发生率 ,凋亡相关基因P53蛋白的表达以及淋巴细胞凋亡发生与疾病活动性的相关性。结果　在IL 1 8刺激培养作用下 ,活动期SLE淋巴细胞凋亡发生率较正常人显著增高 (P <0 .0 1 ) ,而静止期则无明显变化 (P >0 .0 5)。P53蛋白表达在活动期SLE较正常人显著性下降 (P <0 .0 1 ) ,静止期无明显变化 (P >0 .0 5)。P53的表达与疾病活动指数SLEDAI之间有明显的相关性 (P <0 .0 1 )。结论　IL 1 8可引起SLE患者PBL凋亡率的增高 ,表明IL 1 8在体内凋亡或凋亡相关性免疫机制中起着一定的作用     

Presence of antibodies to replication protein A in some patients with systemic lupus erythematosus (SLE)

Presence of antibodies directed against replication protein A (RPA), a DNA binding protein complex composed of three subunits (RPA-70, RPA-32 and RPA-14) was investigated among patients with SLE and other autoimmune diseases using immunoblot analysis to RPA-70 and RPA-32 recombinant proteins. Anti-RPA antibodies were found in two out of 108 sera from SLE patients, one of them showing reactivity against RPA-32 and RPA-70 and the other reacting only against RPA-32. Sera from 108 patients with other autoimmune disorders as well as from 42 healthy control individuals were negative. Thus, the frequency of these antibodies in SLE is estimated to be 2–3%. The study demonstrates that RPA is one target more of the wide array of autoantigens that elicit an immune response in SLE. The presence of anti-RPA autoantibodies seems to be circumscribed to a small number of patients with SLE.     

Preferential elimination of CD28+ T cells in systemic lupus erythematosus (SLE) and the relation with activation-induced apoptosis

CD28 on T cells provides a potent costimulatory signal for T cell activation. Down-regulation of CD28 on peripheral T cells has been reported in certain clinical conditions, but full studies on the mechanism and biological significance have not been performed. Our extensive phenotype analysis of peripheral blood lymphocytes (PBL) from SLE patients revealed that the absolute number of CD28⁺ T cells of both CD4 and CD8 phenotypes was selectively decreased, while that of CD28⁻ T cells was maintained. CD28⁺ T cells from SLE patients exhibited mostly normal proliferative responses to both CD28-dependent and -independent stimulations. In contrast, CD28⁻ T cells were hyporesponsive to anti-CD3 stimulation in both SLE and normal controls. These results implied that the selective decrease of CD28⁺ T cells in SLE does not result from a hyporesponsiveness of CD28⁺ T cells. To investigate the reason for the selective loss of CD28⁺ T cells, we determined the appearance of apoptotic cells in culture with or without anti-CD3 stimulation. Apoptotic cells defined by merocyanine (MC)540 were gradually increased from 12 h to 24 h. Anti-CD3-induced apoptosis of CD28⁺ T cells was significantly accelerated in SLE, whereas apoptosis of CD28⁻ T cells was hardly detected in both SLE and normal controls. Comparative analysis between CD28⁺ and CD28⁻ T cells on CD95 (Fas) and Bcl-2 expression, which are related to activation-induced cell death (AICD), did not show a major difference, although CTLA4, which has been demonstrated to transmit an apoptosis-inducing signal, was expressed only on CD28⁺ T cells. Our results suggest that CD28-mediated costimulation influences T cell susceptibility to AICD and may be involved in T cell lymphopenia in SLE.     

Impairment of the inhibitory effect of sodium on basophil histamine release in patients with systemic sclerosis

It has been demonstrated that Na⁺ down-regulates IgE-dependent and IgE-independent histamine release from basophils of normal subjects. The aim of this study was to evaluate whether Na⁺ exerts its inhibitory effect on basophil histamine release in patients with systemic sclerosis (SSc). Peripheral blood leucocytes were stimulated with anti-IgE, n-formyl-methionyl-leucyl-phenylalanine (fMLP) and IL-3 in the presence of high and low Na⁺ concentrations, and histamine release was measured by a fluorometric method. The dose–response curves of histamine release induced by the above stimuli were similar in SSc patients (n = 15) and in normal subjects (n = 39). Na⁺ removal from the extracellular medium and its isosmotic replacement with choline chloride led to a significant increase of anti-IgE-and fMLP-induced histamine release in normal subjects, but not in SSc patients. In the former population, histamine release induced by an optimal dose of anti-IgE (1/5000) was 26.4 ± 3.1% in high Na⁺ and 59.3 ± 3.5% in low Na⁺ (mean ± s.e.m., P< 0.0001), whereas in the latter population mean histamine release was 20.4 ± 5.1% in high Na⁺ and 15.8 ± 2.9% in low Na⁺ (P NS). A similar trend was observed when basophils were stimulated with fMLP. Na⁺ exerted a dose-dependent inhibitory effect on anti-IgE- and fMLP-induced histamine release in normal subjects, but not in SSc patients. IL-3-induced histamine release from basophils of SSc patients was increased in a low-Na⁺ solution, but to a lesser extent when compared with normal controls. Therefore basophils from normal subjects and SSc patients behave in a different way when stimulated in a low-Na⁺ medium. The inhibitory effect of Na⁺ on basophil histamine release is impaired in SSc patients, and this abnormality could contribute to basophil dysfunction.     

The H3 anti-phospholipid idiotype is found in patients with systemic lupus erythematosus (SLE) but not in patients with syphilis.

The human H3 idiotype, defined by a mouse monoclonal antibody S2.9, is commonly found in patients with SLE where it is correlated with the amount of anti-cardiolipin antibodies. No correlation between the amount of anti-cardiolipin antibody and the H3 idiotype is found in patients with syphilis. Using the S2.9 antibody, serum from each of 10 patients with SLE and eight patients with syphilis was separated into H3-bearing and H3-negative fractions. Comparison of the partition of anti-cardiolipin antibody in these two groups of patients revealed that much of the anti-cardiolipin antibody (44-91%) was found in the H3+ fraction in patients with SLE; in patients with syphilis, virtually none of the anti-cardiolipin antibody was H3+. In patients with SLE, the H3+ fraction contained both IgG and IgM and antibodies of both kappa and lambda light chains. The H3+ fraction was polyspecific and frequently reacted with dsDNA.     

系统性红斑狼疮患者血清BAFF和IL-21的变化及意义

目的：探讨系统性红斑狼疮患者血清BAFF和IL-21水平的变化意义。方法：采用酶联免疫吸附试验的方法（ELISA）对血清中两种物质进行检测。结果：系统性红斑狼疮患者血清BAFF和IL-21高于对照组；狼疮肾炎肾活检组中BAFF随病理改变加重而升高，IL-21在Ⅱ、Ⅲ型、Ⅳ型狼疮肾炎中有升高，但在Ⅳ型中改变最明显；狼疮伴干燥综合症改变组BAFF和IL-21均增加明显；应用糖皮质激素治疗1周后的患者血清BAFF和IL-21水平均呈下降趋势，但以BAFF下降最明显；系统性红斑狼疮患者血清BAFF和IL-21的变化与患者体内的主要免疫指标变化相关；在Ⅳ型狼疮肾炎患者中BAFF和IL-21的变化呈正相关。结论：系统性红斑狼疮患者血清BAFF和IL-21均增加，T、B淋巴细胞异常功能及协同作用在不同脏器的损伤和不同的病理过程中，各自发挥作用的程度不同。     

系统性红斑狼疮患者外周血内皮祖细胞的实验研究

目的探讨系统性红斑狼疮患者外周血内皮祖细胞（EPC）数量、功能是否改变。方法连续选入33例系统性红斑狼疮（SLE）患者做为SLE组,33名门诊健康体检者为对照组。流式细胞分析计量外周血CD34和KDR双阳性细胞,同时原代培养EPC,培养7 d后MTT法检测增殖能力,改良boydon小室法检测迁移能力。结果SLE组外周血EPC数量较对照组显著减少,P〈0.01;SLE组的增殖、迁移能力均较对照组减弱,P〈0.01。结论系统性红斑狼疮患者外周血EPC数量减少,增殖、迁移功能降低,可能是SLE促动脉粥样硬化发生的机制之一。     

Up-regulated expression of Fas antigen (CD95) by peripheral naive and memory T cell subsets in patients with systemic lupus erythematosus (SLE): a possible mechanism for lymphopenia.

Fas antigen (CD95) is a membrane-associated molecule that mediates apoptotic cell death and may play a role in the induction and maintenance of T cell tolerance. To elucidate the involvement of Fas antigen in human autoimmune diseases, we analysed Fas antigen expression by peripheral T cells from patients with SLE and rheumatoid arthritis (RA), using three-colour flow cytometry. Both CD4+ and CD8+ T cells from SLE patients expressed Fas antigen in a higher density than did these cells from healthy donors and from RA patients. Enhancement of Fas antigen density was noted in Fas+CD45RO+ memory T cells from SLE patients. More remarkably, a significant expression of Fas antigen was observed in CD45RO- naive T cells from SLE patients. CD4+CD45RO- T cells from SLE patients co-expressed Fas antigen and early to intermediate activation antigens such as CD25 and CD71, and late activation antigen HLA-DR in only FashiCD4+ naive T cells. Such up-regulation of Fas antigen expression in SLE patients seems to be clinically meaningful, because mean fluorescence intensity (MFI) of Fas antigen on CD4+ T cell subsets inversely correlates with the absolute size of CD4+ T cell subsets in peripheral blood of SLE patients. These results suggest that T cells with increased Fas antigen expression may be highly susceptible to apoptotic cell death, in vivo. A putative mechanism for lymphopenia in SLE patients is discussed.     

Higher anti-heparan sulphate reactivity during systemic lupus erythematosus (SLE) disease exacerbations with renal manifestations; a long term prospective analysis.

Cross-reactive antibodies against heparan sulphate (HS) have been suggested to play a role in initiating renal disease in SLE. Recently, we found that HS-reactivity is mediated by anti-DNA antibodies complexed with DNA and histones. To evaluate the clinical significance of anti-HS reactivity, we studied prospectively a cohort of 72 consecutive SLE patients, of whom 22 experienced 40 exacerbations. In 20 of these exacerbations renal symptoms were present. In these 20 exacerbations significantly higher anti-DNA (median 1:160) and anti-HS (median 1:30) titres were detected compared with exacerbations without renal manifestations (median 1:60 for anti-DNA and negative for anti-HS). There were no correlations with other symptoms of SLE. Anti-HS titres showed a significant correlation with anti-DNA antibody titres (rs = 0.57, P < 0.05). Anti-HS without anti-DNA reactivity was never detected. Some SLE patients showed a high anti-DNA titre without anti-HS reactivity, suggesting that not all anti-DNA antibodies are able to bind to histone/DNA complexes and thus to exhibit anti-HS reactivity. Our findings indicate that anti-HS reactivity is correlated with renal disease in SLE.     

FcγRIIa polymorphism in systemic lupus erythematosus (SLE): no association with disease

An allotypic variant of FcγRIIa, FcγRIIa-HR (FcγRIIa-R131), has been shown in vitroto reduce the capacity of phagocytic cells to bind and internalize IgG-containing immune complexes. Our aim was to determine whether this allotypic variant was associated with susceptibility to SLE and the development of lupus nephritis, as previous studies have suggested. FcγRIIA genotype analysis was performed by amplification refractory mutation system-polymerase chain reaction (ARMS-PCR) in 215 Caucasoid, 70 Afro-Caribbean, and 46 Chinese patients with SLE, and in 259, 77, and 49 ethnically matched controls, respectively. Distribution of FcγRIIa genotypes between the patients and ethnically matched controls was not significantly different in the three populations studied. No association between the FcγRIIa-HR allotype and nephritis was found. Our results suggest that the FcγRIIa-HR allotype is not a major factor predisposing to the development of SLE, or to lupus nephritis.     

Monocyte (macrophage)-specific antibodies in patients with systemic lupus erythematosus (SLE)

Antibodies reactive for monocytes (macrophages) were found in the sera of patients with systemic lupus erythematosus (SLE). These antibodies were preseent in both IgG and IgM fractions and worked under both warm (37°C) and cole (4°C) conditions. These antibodies were specific for monocytes, because cytotoxic antibodies for monocytes were absorbed with monocytes, but not with T cells, B cells, and granulocytes. Furthermore, their specificity is also different from anti-HLA-DR antibody. The presence of these antibodies correlated with the activity of disease. They were found in 12 of 14 active SLE and 7 of 16 inactive SLE patients. The treatment of normal monocytes with these SLE sera and complement resulted in the depletion of their accessory function for T-cell activation and their phagocytic activity. In the previous paper, we reported that the accessory function of monocytes for T-cell activation was impaired in SLE patients. These results suggest that monocyte-specific antibodies play an important role in the pathogenesis of SLE through disturbing the monocyte regulatory function for immune responses.     

Increased frequency of the long (S) allotype of CR1 (the C3b/C4b receptor, CD35) in patients with systemic lupus erythematosus.

The allotypic forms of the C3b/C4b receptor (CR1, CD35) differ in length, in the number of expressed C3b binding sites and thus in their ability to mediate the processing of circulating C3- and C4-bearing immune complexes. We have used a combination of three informative restriction fragment length polymorphisms (RFLPs) to assess the frequencies of the F (most frequent allele comprised of four long homologous repeats (LHR)), S (five LHR) and F' (three LHR) alleles of the C3b/C4b receptor (CR1, CD35) in a French population of patients with systemic lupus erythematosus (SLE) (n = 63) and healthy controls (n = 158). A significantly higher frequency of the S phenotype was observed among patients (51%) as compared with controls (26%). The F' allele was found in 2/61 patients and 1/85 healthy controls, indicating the rare occurrence of the short CR1 allele in SLE. This allele is also extremely rare in the normal population. The overrepresentation of the S long allele among patients is indicative of a genetic linkage between CR1 and susceptibility to SLE.     

Increased production of the third component of complement (C3) by monocytes from patients with systemic lupus erythematosus.

We measured in vitro C3 production by peripheral blood monocytes from patients with systemic lupus erythematosus (SLE), and found it to be significantly greater than that from normal controls. We also found that monocytes from SLE patients with active disease produced a markedly larger amount of C3 than those from SLE patients with inactive disease. Production of C3 by monocytes correlated with serum levels of anti-dsDNA antibodies and inversely correlated with serum C3 levels in SLE patients. Serial measurement of C3 in the culture supernatant from each SLE patient showed that C3 production by monocytes fell in parallel with a decrease of disease activity. The effect of corticosteroids was ruled out as there was no relation between the level of C3 production by monocytes and the dose of prednisolone. This seems to be the first study in which the C3 production was assayed at a cellular level in SLE patients, and this study suggests that the local C3 production is increased in SLE patients.     

Suppression of haematopoiesis by IgG autoantibodies from patients with systemic lupus erythematosus (SLE).

The inhibiting activity of serum on haematopoiesis has been described in patients with SLE. To explore further the features of serum inhibitor, we first examined the suppression of granulocytic and erythroid colony formation in vitro by serum from patients with SLE using methylcellulose culture. The potent inhibiting activity was demonstrated in six of 20 patients. All of these six patients were associated with leukocytopenia and/or anaemia. Five of 10 sera from patients with active SLE suppressed the colony formation of both burst-forming units of erythrocyte (BFU-E) and colony-forming units of granulocyte/macrophage (CFU-GM), and one serum suppressed BFU-E only. IgG fraction isolated from sera with inhibiting activity suppressed colony formation without complement involvement. The elimination of monocytes and lymphocytes from target mononuclear cells did not affect the suppression by the IgG fractions. The suppressive effect was completely eliminated after incubation of the IgG fractions with progenitor-enriched mononuclear cells. Flow cytometric analysis showed these IgG bound to CD34+ haematopoietic progenitor cells, but not to CD33+ cells. These data suggest that (i) the inhibitor of colony formation in serum was observed in IgG fraction; (ii) its suppressive effect on colony formation was mediated by neither monocytes and lymphocytes nor complements; and (iii) IgG fraction could bind to primitive haematopoietic progenitor cells and suppress the growth of these cells. Thus, IgG autoantibodies to primitive haematopoietic progenitor cells are demonstrated to be present in the sera of a significant proportion of active SLE patients with anaemia and leukocytopenia and to suppress the progenitor cell growth.