The results show that in SLE patients, the finding of a relative increase in Con A-bound serum alpha 1-acid glycoprotein is a more sensitive indicator of intercurrent infection than is the finding of increased levels of CRP.
It is not yet known how this genetic polymorphism mediates its effect on CRP expression, and it probably is not a systemic lupus erythematosus susceptibility factor.
To test whether CRP participates in the pathogenesis of systemic lupus erythematosus (SLE), we examined disease development in lupus-prone (NZB x NZW)F(1) (NZB/NZW) mice expressing a human CRP transgene (hCRPtg/BW).
We assess the proposed method using simulated data, and apply it to a polymorphism in the c-reactive protein (CRP) gene typed in families collected to investigate human systemic lupus erythematosus.
Our study was done to confirm the reported association in an independent population-based case-control cohort, and also to investigate the influence of 3 additional CRP tagSNP (-861, -390, +90) on SLE risk and serum CRP concentrations.
Multiple genes may be involved and identifying them will provide an insight into pathways regulating CRP expression, highlight potential cardiovascular disease and SLE candidates and improve the ability of basal CRP to predict cardiovascular risk.
Recently, 2 single-nucleotide polymorphisms (SNP) in the CRP gene (+838, +2043) have been shown to be associated with CRP concentrations and/or SLE risk in a British family-based cohort.
C-reactive protein (CRP) is an acute-phase protein with therapeutic activity in mouse models of systemic lupus erythematosus and other inflammatory and autoimmune diseases.
We have previously reported that lupus monocytes display distinctively differing patterns of C-reactive protein (CRP)-inducing cytokine interleukin (IL)-6, IL-1beta, and tumor necrosis factor (TNF)-alpha secretion when stimulated with either immune complexes (ICs) or lipopolysaccharide (LPS).
We review the available functional and genetic evidence supporting a role for CRP in the pathogenesis of SLE, but recognize that inconsistencies in the existing data mean that conclusions have to be interpreted with caution.
Increased s-BAFF levels in SLE patients are associated with the acute-phase responses, CRP and haemoglobin, but probably not dependent on BAFF genotype or expression.
Significant positive correlation was found between the expression of miR-326 mRNA in Treg cells with CRP and anti-C1q antibody from new-onset SLE patients.2.