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PubMed1994

[A case of systemic lupus erythematosus (SLE) successfully treated with mizoribine (Bredinin)].

Mizoribine, a novel immunosuppressive agent developed in Japan, was administered as a monotherapy to a systemic lupus erythematosus (SLE) patient with the clinical symptoms and immunological abnormalities accompanying SLE showing marked improvement. The result of prolonged administration over 22 months in this case showed neither relapse nor side-effects. Reports have been made about mizoribine used concomitantly with steroids in the treatment of SLE; however, there have not been any reports of mizoribine as a monotherapy for SLE being effective. In this case, mizoribine (150 mg/day) was administered without steroids as a monotherapy on a outpatient basis since the patient's condition overall was relatively good and the serious complications of the heart, kidneys, and lungs that accompany SLE were not observed. The results of this treatment showed improvements in alopecia, arthritis, and systemic malaise from about the 4th week after the start of administration, and the clinical symptoms that accompany SLE had completely disappeared in the 8th week. Also, the immunological tests markedly improved. Four months after the start of administration the immunological abnormalities in the anti-DNA antibody, rheumatoid factor, and immune complex were completely corrected. This case showed dramatic improvement in the SLE clinical symptoms and immunological abnormalities with the mizoribine monotherapy as well as the potential for mizoribine monotherapy to maintain a state of remission over the long term.

Anti-Inflammatory Agents, Non-Steroidal↗

PubMedDate not supplied

Incidence of anti Hsp 90 and 70 antibodies in children with SLE, juvenile dermatomyositis and juvenile chronic arthritis.

OBJECTIVE: To determine the incidence of anti-hsp90 and 70 antibodies in children with SLE, juvenile dermatomyositis and juvenile chronic arthritis. METHODS: We utilized a previously described ELISA to detect the presence of antibodies to mammalian hsp90 and 70 in 33 children with SLE, 55 with juvenile chronic arthritis (JCA) and 11 with dermatomyositis. Sera from 19 children with non-autoimmune conditions served as controls. RESULTS: Antibodies reactive with hsp90 and/or 70 were detected in 35% of the children with SLE, and the numbers of children with SLE who have raised IgG anti-hsp90 antibodies (24%) is very similar to our adult onset cases, although the prevalence of IgM antibodies is much smaller. However, serum antibodies to hsp70 were as infrequent in children with SLE or JCA as in adults with SLE or RA, although IgG antibodies to hsp70 were detected in 50% of the synovial fluid of JCA patients. CONCLUSION: The incidence of antibodies to hsp90 in childhood-onset SLE resembles that described in adult onset disease suggesting that, despite clinical differences between the two, a subset of each may share a similar pathological mechanism of disease.

Adolescent↗

PubMed2002

Evaluation of a new automated enzyme fluoroimmunoassay using recombinant plasmid dsDNA for the detection of anti-dsDNA antibodies in SLE.

ELISA methods to detect anti-double-stranded DNA (anti-dsDNA) antibodies are highly sensitive, but are less specific for the diagnosis of SLE than the immunofluorescence test on Crithidia luciliae (CLIFT) and the Farr assay because they also detect low-avidity antibodies. This study evaluated the specificity, sensitivity, positive predictive value (PPV), and negative predictive value (NPV) of a new automated fluoroimmunoassay (EliA dsDNA; Pharmacia, Freiburg, Germany). We compared the results with those obtained using a commercial CLIFT and an in-house anti-dsDNA IgG ELISA method, and verified its putative ability to detect only high-avidity anti-dsDNA antibodies. Sera from 100 SLE patients and 120 controls were studied. The control group included 20 healthy donors, 70 patients with other rheumatic diseases (32 systemic sclerosis (SSc); 18 primary Sjögren syndrome (pSS), 20 rheumatoid arthritis (RA)), and 30 patients with various infectious diseases (ID). Anti-dsDNA avidity was estimated using an ELISA method based upon the law of mass action, and a simplified Scatchard plot analysis for data elaboration; the apparent affinity constant (Kaa) was calculated and expressed as arbitrary units (L/U). Sensitivity, specificity, PPV, and NPV for SLE were 64%, 95.8%, 93.8% and 72.7%, respectively, for the EliA anti-dsDNA assay; 55%, 99.2%, 98.5%, and 68.8%, respectively, for the CLIFT; and 64%, 93.3%, 90.6%, and 72.3%, respectively, for the in-house ELISA. Although EliA anti-dsDNA was positive mainly in SLE patients with high- (Kaa>80 L/U) and intermediate- (Kaa 30-80 L/U) avidity antibodies (45.3% and 49.9%, respectively), it was also positive in five (7.8%) SLE patients with low-avidity anti-dsDNA antibodies, and five controls (three SSc, one pSS, and one ID) (mean Kaa = 16.4 +/- 9.04 L/U). In conclusion, EliA anti-dsDNA assay showed a higher sensitivity than the CLIFT, and a good specificity and PPV for SLE. Its putative ability to detect only high-avidity anti-dsDNA antibodies remains questionable.

Adult↗

PubMed1995

Comparison of the anti-laminin antibody response in patients with systemic lupus erythematosus (SLE) and parasitic diseases (filariasis).

In this study, we analyzed the presence of antibodies against the basement membrane antigen laminin (LMN) in patients with systemic lupus erythematosus (SLE), filariasis, and normal controls. By ELISA, 13.8% of SLE (12/87), 66.7% of parasitized patients (20/30), and two of the normal controls had these antibodies. IgG1 anti-LMN response was elevated in all groups, whereas IgG2 and IgG3 were also elevated in parasitized patients. The analysis of the IgG anti-laminin binding capacity in SLE and parasitized patients showed similar average antibody affinity. These antibodies did not react with fibronectin by a competition ELISA. By Western blot, the anti-laminin antibodies could be demonstrated in parasitized patient sera but not in SLE sera. Moreover, the ability of these antibodies to bind to heat-treated LMN (100 degrees C for 4 min) was different. The study of the binding capacity with native or denatured LMN by Western blot and dot-blot assays showed that the anti-LMN antibodies from parasitized patients were able to react with both native and denatured forms of LMN, whereas in SLE patients these antibodies were demonstrated only with native LMN. On the other hand, the reactivity detected in the normal control sera seems to be different from the anti-LMN antibodies from SLE and parasitized patients, and probably reflects the existence of natural antibodies in these sera. The presence of anti-LMN antibodies correlates significantly with the ability of inhibition of U937 cell adhesion to LMN-coated surfaces (P < 0.0025). The difference of anti-laminin reactivity suggests that antibodies produced following immunization with autoantigens or similar molecules present in parasites have different specificities from those spontaneously produced by individuals with autoimmune diseases.

Animals↗

PubMed1993

No direct correlation between HLA-DPB1 and antibodies against recombinant Ro (SS-A)/La (SS-B) proteins in systemic lupus erythematosus. SLE Study Group.

We investigated the association of HLA-DPB1 alleles with the occurrence of autoantibodies against Ro (SS-A) or La (SS-B) using recombinant 52 kD-Ro, 60 kD-Ro and La proteins in 177 German patients with systemic lupus erythematosus (SLE). A significant increase in the frequency of DPB1*0101 is observed in SLE patients compared to healthy controls (Pcorr.. < 0.004). Antibodies against 52 kD-Ro, 60 kD-Ro and La are tested by ELISA and are found with a frequency of 25.4%, 33.9% and 17.5% in the patients, respectively. An association with HLA-DPB1*0101 is observed for antibodies against La (P < 0.01) and 52 kD-Ro (P < 0.01), but not for 60 kD-Ro in the absence of La/52 kD-Ro. Since there is a strong linkage disequilibrium between DPB1*0101 and DR3 in the normal population and in SLE patients, and since there is an association between DR3 and SLE, as well as between DR3 and the occurrence of recombinant Ro/La antibodies in SLE patients, we investigated whether DPB1*0101 is associated per se or via linkage disequilibrium with DR3. DPB1*0101 in the absence of DR3 is not more common in patients than in controls and not in patients with autoantibodies to Ro and La than without autoantibodies. We conclude that there is no evidence for a direct involvement of DPB1*0101 in the production of Ro/La autoantibodies in SLE patients.

Alleles↗

PubMed1991

Pathogenesis of SLE: immunopathology in man.

Antibodies against native DNA are not only a disease-specific marker for systemic lupus erythematosus (SLE); in addition, there is good direct evidence that these antibodies also play a major part in pathogenic mechanisms leading to systemic and organ-specific disease manifestations. The origin of anti-dsDNA antibodies is still poorly understood, especially as dsDNA per se is not immunogenic. As recently shown, evidence is now accumulating that anti-dsDNA antibodies are not germline-encoded but antigen-driven, as demonstrated by the establishment of human anti-dsDNA antibody clones from SLE patients and sequence analysis. In sera of SLE patients there is an elevated level of nucleic acids, which indicates that defective clearance mechanisms for nucleic acids are present. The question as to whether these nucleic acids could serve as an antigen has been recently addressed by studies of plasma nucleic acids isolated from circulating immune complexes from SLE patients. These studies indicate that plasma nucleic acids in SLE patients have structures of amino acid sequences which have a striking homology with the gag-pol overlap region of HIV-1. Whether these nucleic acids play a role in the pathogenesis of SLE, indicating the involvement of a retrovirus in the pathogenesis, or whether they rather reflect an amino acid homology with an endogenous human retrovirus family is not yet known.

Antibodies, Antinuclear↗

PubMed1987

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 present in both IgG and IgM fractions and worked under both warm (37 degrees C) and cold (4 degrees 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.

Antibody Specificity↗

PubMed1989

Distribution of anti-F(ab')2 antibodies and the 16/6 idiotype in systemic lupus erythematosus (SLE) probands and kindreds.

Levels of serum anti-F(ab')2 antibodies and expression of the 16/6 anti-DNA idiotype were studied in 103 sera from first-degree relatives of 17 systemic lupus erythematosus (SLE) kindreds. Among healthy SLE relatives, 35.9% showed anti-F(ab')2 elevations and 24%, Id 16/6 expression. Forty-three and two-tenths percent of healthy SLE relatives with elevated anti-F(ab')2 also showed expression of 16/6; when Id 16/6 was positive, 16 of 25 relatives (64%) showed parallel elevations of anti-F(ab')2. However, within individual families, distribution patterns of elevated anti-F(ab')2 and Id 16/6 often did not coincide. Affinity-isolated anti-F(ab')2 from four members of a single SLE kindred showed relative enrichment for Id 16/6 in only two of the four individuals studied. Moreover, none of the isolated anti-F(ab')2 antibodies within this kindred or another kindred showing 16/6 Id expression reacted directly with 16/6 Id. Our studies suggest that whereas both anti-F(ab')2 and Id 16/6 are increased within SLE kindreds, expression of the two does not always coincide. Furthermore, anti-F(ab')2 antibodies do not show direct reactivity with Id 16/6. A number of anti-DNA idiotypic markers may play a role in idiotypic networks among such SLE kindreds.

Adolescent↗

PubMed1992

The presence of antibodies to purified p24gag protein of HTLV-I in sera of patients with systemic lupus erythematosus (SLE).

Sera of patients with systemic lupus erythematosus (SLE) were tested for their reactivity to HTLV-I by western blotting (WB). Seven (18%) of 40 SLE serum samples reacted to the p24gag protein of HTLV-I by WB using purified gag antigens. The specificity of anti-p24gag antibodies in the SLE sera was confirmed by competitive inhibition on WB. Two of the seven patients were shown to be HTLV-I carriers, because HTLV-I infected T cell lines were easily established from their peripheral blood mononuclear cells (PBMC). Except for these two carrier patients, the gag proteins were not detected in the lysates of PBMC by WB using anti-p24gag and anti-p19gag monoclonal antibodies. The gag and pX genes of HTLV-I were not detected by PCR in PBMC of the SLE patients, with the exception of the 2 HTLV-I carrier patients. These results show no direct involvement of HTLV-I in the etiology of SLE. However, the existence of a specific antibody to p24gag in the sera of some of the noncarrier SLE patients suggests a crossreactivity to either unknown viruses or some autoantigens.

Base Sequence↗

PubMed2005

CTLA-4 polymorphisms and systemic lupus erythematosus (SLE): a meta-analysis.

Several reports demonstrate association between variants of the cytotoxic T lymphocyte antigen-4 (CTLA-4) and autoimmune diseases. CTLA-4 may generate autoimmunity by immune dysregulation, making CTLA-4 an attractive candidate gene for systemic lupus erythematosus (SLE) susceptibility. Previous CTLA-4 association studies with SLE, however, have produced inconsistent results. We have performed a meta-analysis to better assess the purported associations. A total of 14 independent studies (to July 2004) testing association between one or more CTLA-4 polymorphisms and SLE were used in this analysis. We have compared allele and genotype frequencies at four polymorphic sites found in exon-1 (at +49), the promoter region (at -318 and -1722), and the 3' untranslated region (3'UTR) (dinucleotide repeat). We have evaluated both fixed and random effect models, depending on the presence of between-study heterogeneity. The data demonstrate that the exon-1 +49 polymorphism is significantly associated with SLE susceptibility. The overall risk, measured by odds ratio (OR), for exon-1 +49 GG genotype is 1.287 [95% confidence interval (CI)=1.031-1.562, P=0.011]. Stratification by ethnicity indicates the exon-1 +49 GG genotype is associated with SLE, at least in Asians (OR=1.293, 95% CI=1.031-1.620, P=0.026). European-derived populations have an effect of similar magnitude (OR=1.268, 95% CI=0.860-1.870, P=0.230), though not significant. Similar trends are found in allele-specific risk estimates and disease association. The OR for the exon-1 +49 risk allele (G) in Asians is 1.246 (95% CI=1.057-1.469, P=0.009), while Europeans have no evidence of allelic association (OR=0.978, 95% CI=0.833-1.148, P=0.780). In conclusion, this meta-analysis supports the CTLA-4 exon-1 +49 (A/G) polymorphism influencing the risk for developing SLE, especially in Asians.

Antigens, CD↗

PubMed2000

Evaluation of cerebrospinal fluid for the presense of anticardiolipin antibodies (aCL) in NP-SLE patients.

Many neurological or psychiatric manifestations of SLE (NP-SLE) are related to the presence of anticardiolipin antibodies (aCL) in the patient's sera. The aim of this study was to evaluate the presence of aCL in cerebrospinal fluid (CSF) in SLE patients with NP features. Fifteen SLE patients were studied, all with NP features. CSF was evaluated for intrathecal IgG synthesis, oligoclonal IgG, and blood-brain barrier impairment. Sera and CSF were tested by ELISA for the presence of aCL-IgG and aCL-IgM with and without beta2 glycoprotein (beta2 GPI) cofactor. CSF and sera of 50 low back pain patients served as controls. Six patients were aCL(+) and nine aCL(-). In all patients the general CSF examination was normal. In all patients the value of indices of intrathecal IgG synthesis were normal but oligoclonal protein was present in the CSF of three patients. In none of the patients was the blood-brain barrier impaired. Neither aCL-IgG nor aCL-IgM was detected in the CSF of any NP-SLE patient. Mean levels of aCL in patients without cofactor beta2 GPI and with cofactor were as follows: for IgG class 0.005 and 0.057 OD (negative); for IgM class 0.004 and 0.024 OD (negative). We could not detect aCL in the CSF of patients with NP-SLE, even if sera were positive for aCL.

Adult↗

PubMed1985

Modulation of the sodium periodate (NaIO4) response in systemic lupus erythematosus (SLE): effect of interleukin-1 (IL-1), interleukin-2 (IL-2), phorbol myristate acetate (PMA), and indomethacin.

The proliferative activity of peripheral blood mononuclear cells (PBMN) from patients with systemic lupus erythematosus (SLE) activated by sodium periodate (NaIO4) is greatly diminished. The effect of the cytokines Interleukin-1 (IL-1) and Interleukin-2 (IL-2) on the NaIO4 reaction was investigated. Addition of IL-1 resulted in partial restoration of the reaction of SLE PBMN to NaIO4, and a similar effect was demonstrated in the presence of phorbol myristate acetate (PMA). Addition of IL-2 to NaIO4 activated SLE PBMN, however, caused a marked improvement in their proliferative activity. The presence of indomethacin resulted in only a slight increase in [3H]thymidine incorporation by the NaIO4-treated SLE cells. The results suggest that the defect in the response of SLE PBMN cells to NaIO4 is due to inadequate availability of IL-1 and IL-2. Excessive production of prostaglandin in SLE might also contribute to the defective response to NaIO4 but does not appear to play a major role.

Female↗

PubMed2004

A new CD21low B cell population in the peripheral blood of patients with SLE.

A hallmark of systemic lupus erythematosus (SLE) is the production of autoantibodies. Recent reports suggest an abnormal peripheral blood B cell homeostasis in SLE patients without being conclusive. We analyzed by four color flow-cytometry peripheral blood B cell subpopulations of SLE patients, healthy donors, and patients with other systemic autoimmune diseases. IgM memory but not switched memory B cells of SLE patients were significantly decreased compared to healthy donors, whereas transitional B cells, characterized by CD19+IgMhiIgD+CD24hiCD38hi, were significantly expanded in SLE patients but also found in other autoimmune disorders. The population of plasmablasts (CD19loCD21loCD27++CD38++) was increased in active disease. Most interestingly, B cells in autoimmune disorders contain a so far uncharacterized subpopulation with an activated phenotype (CD19hiCD21loCD38loCD86int). None of the identified subpopulations was associated with current or previous therapy and therefore may represent different aspects of the disturbed B cell homeostasis in patients with SLE.

Adult↗

PubMed1997

Systemic lupus erythematosus (SLE) lymphadenopathy presenting with histopathologic features of Castleman' disease: a clinicopathologic study of five cases.

Lymph node enlargement is common in active systemic lupus erythematosus (SLE), a disease characterized by well defined clinical criteria. Although numerous reports have described the characteristic histology of SLE lymphadenopathy to include necrotizing lesions and hematoxylin bodies, no detailed description has examined the histopathologic features that are similar to Castleman's disease (CD) in SLE patients. In this report, we describe the clinicopathologic findings of CD-like peripheral lymphadenopathy, which was identified in five (26%) of 19 SLE patients. These five patients were all female with an age range of 24 to 44 years, and four of them presented with multicentric lymphadenopathy. They also had systemic symptoms and abnormal laboratory findings, indicating active disease, although two patients had not fulfilled the diagnostic criteria of SLE at the initial disease. The size of the enlarged lymph nodes seldom exceeded 2.0 cm in diameter, and biopsies revealed histopathologic features similar to CD, of intermediate type in three patients and hyaline vascular type in two according to the classification of Flendrig [7]. Immunohistochemical studies demonstrated polyclonal plasma cell populations in all five cases. Epstein-Barr virus genomes were detected in the small lymphocytes of two of the three cases examined by in situ hybridization studies. Recently, the histopathologic findings of CD have been associated with a disrupted immune response, and the present data suggest that SLE should be listed as one of the diseases showing the histopathologic features similar to CD.

Adult↗

PubMed2003

The effect of IL-12 on clinical and laboratory aspects of experimental SLE in young and aging mice.

IL-12 plays a crucial role in a variety of immune responses that are involved in immuno-senesence and autoimmune diseases. Experimental SLE can be induced in mice by the monoclonal anti-DNA autoantibody bearing the 16/6Id. Aging mice are less susceptible to disease induction. We evaluated the in vivo effects of IL-12 on several parameters related to aging and to experimental SLE. Young (2 months) and aging (10 months) mice that were or were not immunized with the 16/6Id were treated with IL-12. IL-12 treated unimmunized BALB/c and C3H.SW mice had significant elevated levels of anti-DNA antibodies. A high percentage of these mice had glomerular immune complex deposits (ICD). IL-12 treatment resulted in significant increase of IL-1 and IFN-gamma and a decrease of IL-10 production in unimmunized mice. The same IL-12 induced changes were observed in mice with experimental SLE but were less pronounced than in normal mice. In general, all the effects in SLE afflicted mice were more prominent in aging than in young mice. Treatment of mice with experimental SLE upregulated IL-1, IL-2, IFNgamma and downregulated IL-10. These changes were observed in the groups of young as well as old mice. In conclusion, administration of IL-12 to aging mice reversed their Th1/Th2 cytokine profile and thus rendered them vulnerable to the induction of experimental SLE.

Aging↗

PubMed1994

Host-microflora interaction in systemic lupus erythematosus (SLE): colonization resistance of the indigenous bacteria of the intestinal tract.

Experimental data suggest a role for the microflora in Systemic Lupus Erythematosus (SLE). Anti-ds-DNA antibodies may be pathogenic in SLE by forming immune complexes with DNA. Foreign bacteria in the intestines could constitute the stimulus for anti-ds-DNA antibody production in SLE. Colonization Resistance (CR) is the defence capacity of the indigenous microflora against colonization of the intestines by foreign bacteria. A low CR implies increase of translocation of bacteria and a higher chance of subsequent, possibly DNA-cross-reacting antibacterial antibody production. We measured CR by a comprehensive biotyping technique in healthy individuals and patients with inactive and active SLE. CR tended to be lower in active SLE patients than in healthy individuals (P = 0.09, Wilcoxon one sided, with correction for ties). This could indicate that in SLE more and different bacteria translocate across the gut wall due to a lower CR. Some of these may serve as polyclonal B cell activators or as antigens cross-reacting with DNA.

Acute Disease↗

PubMed2000

Urine free light chains in SLE: clonal markers of B-cell activity and potential link to in vivo secreted Ig.

As a marker of in vivo B-cell activity, urine levels of free light chain (FLC) were measured twice weekly by radioimmunoassay (RIA) and correlated with disease activity over periods of 5-10 months in seven patients with systemic lupus erythematosus (SLE). In addition, RIA-measured urine albumin was used to track glomerular injury, and alpha1-microglobulin (alpha1-M) levels, 28- to 32-kDa protein, provided control measurements on excretion of low-molecular-weight proteins. As controls, urine FLC levels were obtained from healthy normals and in subjects with acute pharyngitis, sickle-cell anemia, and acute sepsis or pneumonia. The control results showed that with acute sepsis/pneumonia had marked increases in urine FLC, while pharyngitis and sickle-cell controls had normal FLC levels. In SLE, active patients receiving intravenous cyclophosphamide and high-dose steroids exhibited highly increased urine FLC that fluctuated widely during therapy and fell to normal range levels with disease remission. During active SLE, urine albumin often was increased, while alpha1-M levels remained in normal range. In contrast to the increased FLC of active disease, inactive patients on low-dose maintenance therapy had predominantly normal FLC levels throughout the collection period. These results support our hypothesis that longitudinal levels of urine FLC can be used to track disease-related B-cell activity in SLE. Furthermore, we suggest that the urine FLC of active SLE would share LC idiotype with the clonal associated in vivo secreted Ig, and thus permit the identification of these antibodies that are targeted to the culprit immunogen(s) responsible for the pathogenesis of SLE.

Adult↗

PubMed2006

Meta-analysis of TNF-alpha promoter -308 A/G polymorphism and SLE susceptibility.

Alleles of tumor necrosis factor-alpha (TNF-alpha) gene have been inconsistently associated with systemic lupus erythematosus (SLE), particularly the 308-A/G functional promoter polymorphism. To generate large-scale evidence on whether 308-A/G promoter polymorphism is associated with SLE susceptibility we have conducted a meta-analysis. We have identified 21 studies of this polymorphism and SLE using MEDLINE search. Meta-analysis was performed for genotypes A/A (recessive effect), A/A+A/G (dominant effect), and A allele in fixed or random effects models. All control samples were in Hardy-Weinberg proportion. The overall odds ratio (OR) of the A/A genotype was 3.2 (95% CI=2.0-5.3, P<0.001). Stratification by ethnicity indicated that the A/A genotype was associated with SLE in European-derived population (OR=4.0, CI=2.5-6.4, P<0.001). No association was detected in Asian-derived population (OR, 1.3, CI=0.3-6.3, P=0.76). The overall OR for the risk genotypes (A/A and A/G) was 2.0 (CI=1.3-3.1, P<0.001). Similar results were found between the risk allele A and SLE where a significant association was found in European population (OR=2.1, CI=1.6-2.7, P<0.001), but not in Asian (OR=1.4, CI=0.8-2.3, P=0.2) or African (OR=1.2, CI=0.6-2.5, P=0.59) populations. In summary, this meta-analysis demonstrates that the TNF-alpha promoter -308 A/G polymorphism may confer susceptibility to SLE, especially in European-derived population.

Alleles↗