Using RT-PCR methods, IL-6 mRNA was detected in the glomeruli of renal biopsy specimens obtained from patients with IgA nephropathy and lupus nephritis.
We investigated mRNA expression for medullasin (an inflammatory serine protease in bone marrow cells) in peripheral blood mononuclear cells (PBMC) obtained from 36 patients with primary IgA nephropathy (IgAN), 30 patients with other types of primary glomerular disease, 18 patients with secondary IgA nephritis including lupus nephritis and hepatic glomerulosclerosis and 24 healthy age-matched controls.
In patients with active lupus nephritis, urinary MCP-1 was significantly higher than in lupus patients studied in the inactive phase of the disease or in healthy volunteers.High doses of i.v. methylprednisolone significantly lowered urinary MCP-1 in patients with active lupus nephritis.
The number of intraglomerular cells positive for Fas antigen was high in Henoch-Schönlein purpura nephritis and lupus nephritis, and that of Bcl-2-positive intraglomerular cells was high in lupus nephritis, focal glomerular sclerosis, and IgA nephritis.
These observations suggest that MCAF is probably involved in the pathogenesis of LN with active lesions, possibly through the recruitment and activation of M phi, and that measurement of urinary MCAF levels may be a useful clinical tool for monitoring the disease activity of LN.
Therefore, since immune complex clearance is essential in SLE, we hypothesized that Fc gamma RIIA genes are important disease susceptibility factors for SLE, particularly lupus nephritis.
These observations suggest that MCAF is probably involved in the pathogenesis of LN with active lesions, possibly through the recruitment and activation of M phi, and that measurement of urinary MCAF levels may be a useful clinical tool for monitoring the disease activity of LN.
This study was designed to evaluate the role of TNF production of peripheral blood mononuclear cells (PBMC) and its association with TNFB gene polymorphism in SLE, particularly lupus nephritis.
The relationship between expression of TGF-beta 1 protein or TGF-beta 1 mRNA and tissue damage was investigated using the enzyme-antibody and in situ hybridization method in frozen slices of renal tissue from 30 patients: 25 with glomerulonephritis (18 with immunoglobulin A nephropathy; two with focal glomerulosclerosis, one with membranous nephropathy, one with crescentic glomerulonephritis and three with lupus nephritis) and five control patients with minimal change disease.
The mRNA expression of PDGF-B and PDGFR-beta was significantly increased in the glomeruli of patients with mesangial proliferative glomerulonephritis (IgA nephropathy, Henoch-Schönlein purpura nephritis, and lupus nephritis) compared with those in normal glomeruli.
This study was designed to evaluate the role of TNF production of peripheral blood mononuclear cells (PBMC) and its association with TNFB gene polymorphism in SLE, particularly lupus nephritis.
Universally binding nucleosomal epitopes are productively recognized by autoreactive T cells by binding to the T-cell receptor-alpha chain; (b) circulating T cells from patients with lupus commonly display a deficiency of the T-cell receptor zeta chain, and upon ligation of their cell-surface antigen receptor overproduce tyrosine phosphorylated proteins; (c) lupus and lupus nephritis are associated with a low-binding FcgammaRIIIA (CD16) polymorphism that crosses ethnic barriers; (d) the pathogenetic role of the cytokine interleukin-10 is expanding, because it is reportedly overproduced not only by cells from lupus patients but also by cells from their healthy relatives, and its overproduction in vitro is correlated with increased apoptotic cell death and with lymphopenia.
In human SLE, genes of early components of complements as well as many polymorphic genes (including the MHC class II and class III, FcgammaR, mannose-binding protein, IL-6, Bcl-2, and IL-10 genes) have been associated with SLE or LN by population-based case-control or within-case studies.
Universally binding nucleosomal epitopes are productively recognized by autoreactive T cells by binding to the T-cell receptor-alpha chain; (b) circulating T cells from patients with lupus commonly display a deficiency of the T-cell receptor zeta chain, and upon ligation of their cell-surface antigen receptor overproduce tyrosine phosphorylated proteins; (c) lupus and lupus nephritis are associated with a low-binding FcgammaRIIIA (CD16) polymorphism that crosses ethnic barriers; (d) the pathogenetic role of the cytokine interleukin-10 is expanding, because it is reportedly overproduced not only by cells from lupus patients but also by cells from their healthy relatives, and its overproduction in vitro is correlated with increased apoptotic cell death and with lymphopenia.
A dramatic increase in PAI-1 activity in plasma and in PAI-1 mRNA in the kidneys was observed in both models, and this increase appeared to correlate with fibrin deposition in the renal microvasculature and with the progression of lupus nephritis.
To evaluate the possibility that intrarenal T cells result from the expansion of lymphocytes using limited T-cell receptor (TCR) genes, we analyzed the TCR Vbeta gene expression among infiltrating lymphocytes in renal tissue compared with simultaneous peripheral blood lymphocytes of four children with new-onset SLE nephritis.