Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lupus nephritis is a major predictor of the prognosis of systemic lupus erythematosus (SLE). The present paper discusses lupus nephritis from clinical and immunopathological points of view. Although recent advances in diagnosis and treatment improve the prognosis of children with SLE, there remain many unsolved clinical problems. One of the current topics in the treatment for SLE is intermittent intravenous cyclophosphamide therapy which is effective even for the steroid-resistant patients with severe lupus nephritis, at least for short-term observation. Immunopathologically, the following issues are discussed: (i) The C5b-9 terminal complement complex plays an important role in the pathogenesis of lupus nephritis. The possible interaction of vitronectin and SP-40,40 is also mentioned; (ii) A semi-quantitative analysis of the charge barrier of the glomerular basement membrane reveals that the charge barrier dysfunction plays an important role in the pathogenesis of proteinuria in lupus nephritis. This study also demonstrates that the charge of immune deposits is important for the initiation of glomerular injury in lupus nephritis; (iii) It is demonstrated that the histopathological diversity of lupus nephritis is based on biological properties of nephritogenic auto-antibodies in murine lupus models.
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PMID:Current topics in childhood lupus nephritis. 825 34

Linkage studies on human families suggest that receptors for the Fc fragments of immunoglobulin G (IgG) (FcgammaRs) could be implicated in the susceptibility to, or the progression of, some autoimmune diseases. In this work we analyse the possible role of polymorphic variants of FcgammaRIIA, FcgammaRIIIA and FcgammaRIIIB genes in the susceptibility to systemic lupus erythematosus, the prototype systemic autoimmune disease. A total of 276 Spanish patients (34 male and 242 female) with systemic lupus erythematosus were included in this cross-sectional study. The FcgammaRIIA-131, FcgammaRIIIA-176 and FcgammaRIIIB-NA1/NA2 polymorphisms were investigated in the patient group as well as in 194 ethnically matched controls using polymerase chain reaction-amplification refractory mutation system (PCR-ARMS). Statistical comparisons of genotype frequencies were performed using the chi2 test. In the case of the FcgammaRIIIB-NA1/NA2 polymorphism, an increase in the frequency of homozygous NA2/NA2 in patients was found (61.2 vs. 51.0%; P = 0.03; OR = 1.5; 95% CI = 1.03-2.24), as well as a decrease in the frequency of the NA1/NA2 genotype (28 vs. 38.7%; P = 0.02; OR = 0.6; 95% CI = 0.41-0.92). These associations were independent of patient gender and HLA-DRB1 specificities. With respect to the FcgammaRIIA-131 and FcgammaRIIIA-176 polymorphisms, no differences were found between patients and controls. Patient stratification according to their lupus-related nephritis status gave similar genotypic distribution patterns in both disease categories in all the cases.
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PMID:FcgammaRIIA, FcgammaRIIIA and FcgammaRIIIB polymorphisms in Spanish patients with systemic lupus erythematosus. 1212 Dec 75

Polymorphisms of FcgammaR have been proposed as genetic factors that influence susceptibility to SLE. FcgammaRIIIB polymorphism in systemic lupus erythematosus (SLE) have been studied in various populations, but the results were inconsistent. The aim of this study was to determine the association of FcgammaRIIIB polymorphism in Korean lupus patients. One-hundred and eighty-three SLE patients (166 female, 17 male) meeting 1982 ACR criteria and 300 Korean disease-free controls were enrolled. Genotyping for the FcgammaRIIIB NA1/NA2 was performed by PCR of genomic DNA using allele-specific primers. There was no significant skewing in the distribution of the three FcgammaRIIIB genotypes, and alleles between SLE and the controls. The frequency of FcgammaRIIIB genotypes in SLE patients and controls was FcgammaRIIIB NA1/NA1 27.9% versus 26%, NA1/NA2 55.2% versus 51.7%, NA2/NA2 16.9% versus 22.3%, respectively. The gene frequencies of NA1 allele were 0.56 in the SLE and 0.52 in controls, respectively. Among clinical manifestations, thrombocytopenia was more common in FcgammaRIIIB NA2/NA2 genotype (P = 0.04, OR 2.4, 95% CI 1.0-5.4), and NA2 allele (P = 0.03, OR 1.7, 95% CI 1.1-2.8). Although FcgammaRIIIB polymorphism was not associated with the development of SLE in Korean, thrombocytopenia was associated with FcgammaRIIIB NA2/NA2 genotype, and NA2 allele.
Lupus 2005
PMID:The association between fcgammaRIIIB polymorphisms and systemic lupus erythematosus in Korea. 1593 33

The aim of this study was to explore whether polymorphisms of the Fcgamma receptors (FcgammaRs) IIB T/I232 and FcgammaRIIIB NA1/NA2, confer susceptibility to systemic lupus erythematosus (SLE) and lupus nephritis (LN). The authors conducted a meta-analysis on associations between the FcgammaRIIB T/I232 and FcgammaRIIIB NA1/NA2 polymorphisms and SLE and LN susceptibility as determined using 1) allele contrast, 2) recessive, 3) dominant models and 4) contrast of homozygotes. A total of 16 separate comparisons were considered, consisting of 2887 SLE patients and 3105 controls. Meta-analysis of the FcgammaRIIB T/I232 polymorphism showed a significant association between the FcgammaRIIB T allele and the risk of developing SLE compared with the FcgammaRIIB I allele (OR = 1.207, 95% CI = 1.061-1.373, P = 0.004). In subjects of Asian descent, a significant association was observed between the FcgammaRIIB T allele and SLE (OR = 1.332, 95% CI 1.138-1.558, P < 0.001). However, in Europeans no such association was found. In contrast, no association was found between SLE or LN and the FcgammaRIIIB NA1/NA2 polymorphism in all subjects, or in European and Asian populations. This meta-analysis shows that the FcgammaRIIB T/I232 polymorphism confers susceptibility to SLE, especially in Asian-derived populations.
Lupus 2009 Jul
PMID:Fcgamma receptor IIB and IIIB polymorphisms and susceptibility to systemic lupus erythematosus and lupus nephritis: a meta-analysis. 1950 69