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

This study assessed the expression of complement receptor 1 (CR1), decay accelerating factor (DAF) and membrane inhibitor of reactive lysis (CD59) on the erythrocytes and glomerulus of diffuse proliferative glomerulonephritis (DPGN) of systemic lupus erythematosus (SLE) patients using flow cytometry and immunofluorescence techniques to elucidate their role in the pathogenesis of DPGN. Expression of CR1 on the erythrocytes and glomerulus of DPGN patients was reduced compared with expression in normal subjects. However, expression of DAF and CD59 was increased on both erythrocytes and glomerulus of DPGN patients, suggesting the generation of a protective response against complement-mediated injury.
Lupus 2000
PMID:Expression of complement regulatory proteins in diffuse proliferative glomerulonephritis. 1078 10

The decline in the levels of erythrocyte complement receptor 1 (ECR1) in systemic lupus erythematosus (SLE) has been widely reported. The most probable cause for this decline is excessive proteolytic shedding of CR1 from the cell surface. Similarly a decline in glomerular CR1 (GCR1) has also been reported in SLE. Because CR1 is excreted in urine it is imperative to study the relationship of urinary CR1 (uCR1) with ECR1 and GCR1, and their overall correlation with disease activity. We have determined the levels of uCR1, ECR1 and GCR1 in SLE patients and compared them with normal controls and minimal change disease (MCD) patients. We found a significant decline in both uCR1 and GCR1 in SLE but not in MCD; levels of uCR1 in MCD were either comparable to those of controls or higher. Immunofluorescence for GCR1 was very high in MCD. We did not find any correlation between ECR1, uCR1 and kidney function tests on divariate scatter analyses. The correlation coefficient for uCR1 and GCR1 was highly significant and positive. Our findings thus suggest that uCR1 reflects the levels of GCR1 expression, which decline drastically in SLE. Therefore we envisage uCR1 as a potential marker for glomerular involvement in SLE.
Lupus 2004
PMID:Modulation of urinary CR1 in systemic lupus erythematosus. 1517 57

Studies performed during the past several decades have demonstrated a role for the complement system in both the etiology and pathogenesis of systemic lupus erythematosus (SLE). However the specifically defective molecular and cellular pathways responsible for the disease and its complications have generally not been identified. In this report, we describe two recent advances in complement pathobiology that highlight future directions for promising investigation toward enhancing our capacity to diagnose SLE, to monitor activity of the disease, and to identify molecular and cellular defects in SLE that can be targeted by therapeutic inhibitors of complement activation. In the first example, we describe recently developed assays to detect erythrocyte C4d and complement receptor 1 for diagnosis and monitoring of disease activity in SLE. In the second example, we describe a recently discovered role for complement in mediating fetal loss in antiphospholipid syndrome and discuss the potential for this observation to facilitate identification and development of complement based biomarkers to predict poor fetal outcome in pregnant patients with SLE. These two examples are meant to underscore the importance of complement in the etiology and pathogenesis of SLE and its complications, and to stress the need for further investigation focused on the link between the complement system and SLE.
Lupus 2004
PMID:New insights into complement: a mediator of injury and marker of disease activity in systemic lupus erythematosus. 1523 Feb 82

The reduced level of complement receptor 1 (CR1) on erythrocytes is speculated as a key mechanism contributing to immune complex (IC) overload and exaggerated complement (C) activation in systemic lupus erythematosus (SLE). Comparatively, fewer studies documented lower levels of CR1 on leukocytes and glomerular podocytes in this disease. The decline in E-CR1 is largely believed as an acquired phenomenon caused due to the proteolytic cleavage of CR1 from erythrocyte membrane. The mechanism underlying reduced CR1 expression on nucleated cells is under constant investigation. Recently, reduced leukocytes CR1 gene transcription had been demonstrated in SLE and was suggested as the main cause of decline in leukocyte CR1 (L-CR1). The relationship of L-CR1 gene transcription with severity and pathophysiology of disease needs to be elucidated. We determined the levels of L-CR1 in 30 active SLE patients and compared with normal healthy controls (n = 30). Patients were categorized into two groups i.e., with nephritis (n = 14) or without nephritis (n = 16). The expression of L-CR1 at transcriptional level was correlated with the levels of serum CIC, C3 and anti dsDNA antibodies. The levels of L-CR1 transcription were significantly reduced in all SLE patients as compared to controls (P < 0.001). This decline in L-CR1 however, was more marked in patients with nephritis than those without nephritis. In addition, the serum levels of CIC, anti dsDNA antibodies were higher and the levels of serum C3 were lower than the normal range in the patients. The difference was much more marked in SLE patients with nephritis than those without nephritis. The levels of L-CR1 transcription correlated negatively with the levels of CIC and anti dsDNA antibodies and positively with serum C3 levels. Thus, between SLE patients with and without nephritis, we found significant difference in the levels of L-CR1 transcription (P < 0.01), CIC (P < 0.05), anti dsDNA antibodies (P < 0.01) and C3 (P < 0.01). Our findings suggest that L-CR1 is drastically reduced in patients with severe form of SLE, i.e., lupus nephritis. Determination of L-CR1 expression at transcriptional level in addition to disease hallmarks like C3, CIC and anti-dsDNA antibodies may facilitate the assessment of severity of SLE and discrimination between patients with or without renal involvement.
Lupus 2005
PMID:Association of leukocyte CR1 gene transcription with the disease severity and renal involvement in systemic lupus erythematosus. 1586 13