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Polymorphisms in STK17A gene are associated with systemic lupus erythematosus and its clinical manifestations 总被引:1,自引:0,他引:1
Andréia Maria da Silva Fonseca Jaqueline de Azevedo Silva João Alexandre Trés Pancotto Eduardo Antônio Donadi Ludovica Segat Sergio Crovella Paula Sandrin-Garcia 《Gene》2013
Systemic lupus erythematosus (SLE) is an autoimmune disorder with several clinical manifestations. SLE etiology has a strong genetic component, which plays a key role in disease's predisposition, as well as participation of environmental factors, such and UV light exposure. In this regard, we investigated whether polymorphisms in STK17A, a DNA repair related gene, encoding for serine/threonine-protein kinase 17A, are associated with SLE susceptibility. A total of 143 SLE patients and 177 healthy controls from Southern Brazil were genotyped for five STK17A TagSNPs. Our results indicated association of rs7805969 SNP (A and G/A genotype, OR = 1.40 and OR = 1.73, respectively) with SLE predisposition and the following clinical manifestations: arthritis, cutaneous and immunological alterations. When analyzing haplotypes distribution, we found association between TGGTC, TAGTC and AAGAT haplotypes and risk to develop SLE. When considering clinical manifestations, the haplotypes TGGTT and TAGTC were associated with protection against cutaneous alterations and the haplotype TAGTC to hematological alterations. We also observed association between SLE clinical manifestations and ethnicity, with the European-derived patients being more susceptible to cutaneous and hematological alterations. 相似文献
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R Suenaga P A Munoz S W Bright N I Abdou 《Journal of immunology (Baltimore, Md. : 1950)》1988,140(10):3508-3514
Spontaneous shift in Id expression of polyclonal anti-DNA antibodies in a patient, BS, with SLE was investigated. BS had active lupus nephritis in 1982 and developed central nervous system lupus in 1986 without evidence of active nephritis. Two rabbit polyclonal anti-Id (BS-82 and BS-86 R-anti-Id) were raised against affinity-purified anti-DNA antibodies prepared from 1982 serum (BS-82) and 1986 serum (BS-86), respectively. In addition, murine monoclonal anti-Id was prepared against BS-82 Id. Direct binding assays showed that all three anti-Id had preferential binding to the immunizing anti-DNA antibodies (the homologous Id) and poor binding to anti-DNA antibodies prepared from the different dated sample of BS. This was confirmed by inhibition assays of binding of anti-Id to the homologous Id by various Id. Moreover, inhibition assays of binding of various Id to DNA by the R-anti-Id showed that the R-anti-Id was the most effective inhibitor for the homologous Id. Testing for Id expression in serial (1982 to 1986) serum samples of BS with the R-anti-Id as probes showed that BS-82 Id declined and was undetectable after October, 1984, whereas BS-86 Id was first detectable in July, 1985, and increased by June, 1986. These results clearly demonstrate spontaneous shifts in Id expression of human anti-DNA antibodies. The phenomenon of Id shift should be considered in any future strategy for the diagnosis and therapy of human autoimmune disease by anti-Id. 相似文献
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Conti F Alessandri C Bompane D Bombardieri M Spinelli FR Rusconi AC Valesini G 《Arthritis research & therapy》2004,6(4):R366-R372
This study was performed to determine the correlation between psychiatric manifestations and several autoantibodies that might
participate in the pathogenesis of psychiatric disorders in the course of systemic lupus erythematosus (SLE). Fifty-one unselected
outpatients with SLE were enrolled. Psychiatric evaluation was performed according to the Diagnostic and Statistical Manual
of Mental Disorders, 4th edition. The prevalence of antibodies against endothelial cells (AECA), cardiolipin, β2 glycoprotein
I, Ro, Ro52, La, glial fibrillary acidic protein, ribosomal P protein, dsDNA, and nucleosomes was assessed by experimental
and commercial enzyme-linked immunosorbent assays. According to the cutoff value, AECA were present in 11 of 17 (64.7%) SLE
patients with psychosis and mood disorders and in 10 of 34 (29.4%) patients without psychiatric manifestations other than
anxiety (P = 0.03). Moreover, the AECA binding index was significantly higher in the first group (P = 0.03). Conversely, no significant correlation was found between the presence of the other autoantibodies studied and psychiatric
involvement. The results of this study suggest a relationship between AECA and psychosis and mood disorders in SLE, supporting
the hypothesis of a biological origin of these disturbances. 相似文献
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V Agnello M M De Bracco H G Kunkel 《Journal of immunology (Baltimore, Md. : 1950)》1972,108(3):837-840
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R. A. Barker 《BMJ (Clinical research ed.)》1989,299(6693):245-247
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V. M. Oh 《BMJ (Clinical research ed.)》1992,305(6860):1000
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Immunoregulatory aberrations in systemic lupus erythematosus. 总被引:48,自引:0,他引:48
A S Fauci A D Steinberg B F Haynes G Whalen 《Journal of immunology (Baltimore, Md. : 1950)》1978,121(4):1473-1479
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EBV and systemic lupus erythematosus: a new perspective 总被引:6,自引:0,他引:6
Gross AJ Hochberg D Rand WM Thorley-Lawson DA 《Journal of immunology (Baltimore, Md. : 1950)》2005,174(11):6599-6607
We have proposed that EBV uses mature B cell biology to access memory B cells as a site of persistent infection. A central feature of this model is that EBV adapts its gene expression profile to the state of the B cell it resides in and that the level of infection is stable over time. This led us to question whether changes in the behavior or regulation of mature B cells would alter the state of EBV persistence. To investigate this, we studied the impact of systemic lupus erythematosus (SLE), a disease characterized by immune dysfunction, on EBV infection. We show that patients with SLE have abnormally high frequencies of EBV-infected cells in their blood, and this is associated with the occurrence of SLE disease flares. Although patients with SLE have frequencies of infected cells comparable to those seen in immunosuppressed patients, in SLE the effect was independent of immunosuppressive therapy. Aberrant expression of viral lytic (BZLF1) and latency (latency membrane proteins 1 and 2a) genes was also detected in the blood of SLE patients. We conclude that the abnormal regulation of EBV infection in SLE patients reflects the sensitivity of the virus to perturbation of the immune system. 相似文献
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Carlsson A Wuttge DM Ingvarsson J Bengtsson AA Sturfelt G Borrebaeck CA Wingren C 《Molecular & cellular proteomics : MCP》2011,10(5):M110.005033
Systemic lupus erythematosus (SLE) and systemic sclerosis (SSc) are two severe autoimmune connective tissue diseases. The fundamental knowledge about their etiology is limited and the conditions display complex pathogenesis, multifaceted presentations, and unpredictable courses. Despite significant efforts, the lack of fully validated biomarkers enabling diagnosis, classification, and monitoring of disease activity represents significant unmet clinical needs. In this discovery study, we have for the first time used recombinant antibody microarrays for miniaturized, multiplexed serum protein profiling of SLE and SSc, targeting mainly immunoregulatory proteins. The data showed that several candidate SLE-associated multiplexed serum biomarker signatures were delineated, reflecting disease (diagnosis), disease severity (phenotypic subsets), and disease activity. Selected differentially expressed markers were validated using orthogonal assays and a second, independent patient cohort. Further, biomarker signatures differentiating SLE versus SSc were demonstrated, and the observed differences increased with severity of SLE. In contrast, the data showed that the serum profiles of SSc versus healthy controls were more similar. Hence, we have shown that affinity proteomics could be used to de-convolute crude, nonfractionated serum proteomes, extracting molecular portraits of SLE and SSc, further enhancing our fundamental understanding of these complex autoimmune conditions. 相似文献