SYSTEMIC LUPUS ERYTHEMATOSUS: PROTOTYPE OF IMMUNE COMPLEX NEPHRITIS IN MAN

1971 ◽  
Vol 134 (3) ◽  
pp. 169-179 ◽  
Author(s):  
D. Koffler ◽  
V. Agnello ◽  
R. Thoburn ◽  
H. G. Kunkel
Keyword(s):  
Immune Complex ◽  
Lupus Erythematosus ◽  
Dna Complexes ◽  
Immunofluorescence Studies ◽  
Serological Studies ◽  
Glomerular Deposits ◽  
Complex Deposition ◽  
Definition Of ◽  
Antigen Antibody ◽  
Insight Into

Serological studies, immunofluorescence studies, and immunochemical assays of glomerular eluates indicate that several antigen-antibody systems may be involved in the pathogenesis of the tissue lesions of SLE. The NDNA-anti-NDNA system appears to be operative in most patients with active SLE. In addition, antibodies to SDNA are found with considerable frequency in SLE sera and glomerular eluates. It is not known if these antibodies fix to NDNA which has been denatured after deposition in glomeruli or if SDNA-anti-DNA complexes are deposited initially. NDNA antigen has been demonstrated in both serum and glomerular deposits, and SDNA determinants have also been found in glomerular deposits. In addition, there is evidence that rheumatoid factor contributes to the immune complex deposition in certain patients either by fixing to preformed immune complexes or as part of an independent γ-globulin-anti-γ-globulin system. It is anticipated that the definition of these immune systems, and the assessment of their relative toxicity will provide insight into underlying etiologic factors as well as provide a sound basis for therapy in this form of glomerulonephritis.

scholarly journals Features of systemic lupus erythematosus in mice injected with bacterial lipopolysaccharides: identificantion of circulating DNA and renal localization of DNA-anti-DNA complexes.

1977 ◽  
Vol 145 (5) ◽  
pp. 1115-1130 ◽  
Author(s):  
S Izui ◽  
P H Lambert ◽  
G J Fournié ◽  
H Türler ◽  
P A Miescher
Keyword(s):  
Immune Complex ◽  
Lupus Erythematosus ◽  
Immune Complexes ◽  
Basement Membranes ◽  
Circulating Dna ◽  
Dna Complexes ◽  
Renal Glomeruli ◽  
Glomerular Deposits ◽  
Dna Antibodies ◽  
Similar Density

After injection of lipopolysaccharides (LPS) in mice, there is first a release of DNA into plasma and secondly an induction of anti-DNA antibodies. The circulating DNA was purified from plasma and physico-immunochemically characterized. This DNA has a similar density to mammalian cellular DNA,is 4--6S insize, and probably represents a mixture of single-stranded DNA (SSDNA) and double-stranded DNA (DSDNA) or DSDNA with some single-stranded regions. This purified DNA was shown to react with anti-DNA antibodies which appeared as early as 3 days after a single injection of LPS in mice. In serum, DNA-anti-DNA complexes were not detected, although unidentified circulating immune complex-like material was demonstrated 5-8 days after the injection of LPS. In tissues, particularly in renal glomeruli, fine granular immune complex-type immunoglobulin deposits appeared along the glomerular capillary walls and in the mesangium 3 days after the injection of LPS. There is a direct correlation between the level of anti-DNA antibodies and the intensity of glomerular deposits and about 40% of immunoglobulins eluted from kidneys are anti-DNA antibodies, indicating that some of the immune complexes localized in kidneys are DNA-anti-DNA complexes. Based on these observations, the following hypothetical mechanism for the glomerular localization of DNA-anti-DNA complexes after the injection of LPS in mice is proposed. First, DNA, which has been released in circulating blood after injection of LPS, might bind to renal glomeruli, probably on glomerular basement membranes (GBM) through a high affinity of GBM for DNA; secondly, circulating anti-DNA antibodies, which appear later, might react with the glomerular-bound DNA and form immune complexes independently of circulating immune complexes. However, the possibility of direct deposition of immune complexes is not ruled out.

Nephrotic Syndrome Associated with Varicella Infection

PEDIATRICS ◽  
1985 ◽  
Vol 75 (6) ◽  
pp. 1127-1131
Author(s):  
Ching-Yuang Lin ◽  
Hey-Chi Hsu ◽  
Han-Yang Hung
Keyword(s):  
Nephrotic Syndrome ◽  
Immune Complex ◽  
Alternative Pathway ◽  
Virus Antigen ◽  
Varicella Infection ◽  
Immune Complex Glomerulonephritis ◽  
Varicella Virus ◽  
Complex Deposition ◽  
Properdin Factor B ◽  
Antigen Antibody

A 4-year-old boy developed nephrotic syndrome following varicella infection. Serologic studies during the early phase of the disease demonstrated a decrease in serum C3, C4, and properdin factor B. Renal biopsy revealed an acute proliferative glomerulonephritis with deposition of immunoglobulins A (IgA) and M, C3, Clq, and varicella virus antigen in the glomerulus, suggesting an immune complex deposition. Ultrastructurally, this suggested a postinfectious immune complex glomerulonephritis. These phenomena suggested that varicella virus antigen antibody complexes were deposited in the glomerulus and activated the classic and alternative pathway of complements, leading to an immune complex glomerulonephritis. During the nephrotic phase, an increase in OKT8 cells and decrease of the OKT4 cells were demonstrated. Two months later, this alteration returned to normal as the renal disease was in remission. This change of lymphocyte subsets during varicella infection may play a role in the pathogenesis of nephrotic syndrome.

Immune complexes: characteristics, clinical correlations, and interpretive approaches in the clinical laboratory.

1982 ◽  
Vol 28 (6) ◽  
pp. 1259-1271 ◽  
Author(s):  
S E Ritzmann ◽  
J C Daniels
Keyword(s):  
Immune Complex ◽  
Lupus Erythematosus ◽  
Immune Complexes ◽  
Complex Disease ◽  
Clinical Medicine ◽  
Clinical Laboratory ◽  
Therapeutic Monitoring ◽  
Serum Samples ◽  
Complement Components ◽  
Antigen Antibody

Abstract Immune-complex-mediated injury is thought to play a role in diseases such as rheumatoid arthritis, systemic lupus erythematosus, serum sickness, various infectious diseases, and malignancies. With increased appreciation of the biological and pathological significance of circulating immune complexes has come efforts to develop appropriate techniques for identifying and measuring them. Common approaches exploit such phenomena as the attachment of complement components to antigen-antibody complexes, the presence of specialized receptors for immune complexes at the surface of cells, and the ability of rheumatoid factor to bind with immune complexes. This variety of assay systems for immune complexes has yielded abstruse results in numerous human pathological conditions. Unfortunately, these results seldom correlate with one another in a given disease. Thus, use of a panel of immune complex assays has been recommended. Indirect consequences of immune complex disease may still be appraised and evaluated with some confidence in clinical medicine: measurements of C3 and C4, cryoglobulins, serum viscosity, and turbidity of serum samples. Measurement of immune complexes may be useful in diagnosis, prognosis, and therapeutic monitoring, but it is the characterization of immune complexes that holds the greatest potential for better understanding of disease mechanisms.

Immune-mediated tubulointerstitial nephritis

2018 ◽  
Author(s):  
Liviu Segall ◽  
Adrian Covic
Keyword(s):  
Immune Complex ◽  
Lupus Erythematosus ◽  
Interstitial Fibrosis ◽  
Tubular Atrophy ◽  
Immunoglobulin G4 ◽  
Immune Mediated ◽  
Inflammatory Bowel ◽  
Complex Deposition ◽  
Stage Renal Disease ◽  
End Stage

Immune-mediated tubulointerstitial nephritides (TINs) are generally encountered in the context of systemic or extrarenal autoimmune diseases, such as sarcoidosis, Sjögren syndrome, systemic lupus erythematosus, inflammatory bowel disease, TIN and uveitis (TINU) syndrome, and immunoglobulin G4-related disease. The pathogenesis of these TINs is complex and more or less unclear; it usually involves leucocyte activation, autoantibodies, immune complex deposition, complement activation, and release of inflammatory cytokines and growth factors. Tubulointerstitial inflammation most commonly has a chronic pattern, although acute forms of TIN may also occur. Furthermore, inflammation may be granulomatous (as in sarcoidosis or Crohn’s disease) or non-granulomatous. Immunofluorescence staining can sometimes reveal immune complex deposits and even antitubular basement membrane autoantibodies. Systemic immunosuppressive therapies are almost always required to prevent progression to irreversible interstitial fibrosis, tubular atrophy, and end-stage renal disease.

Polyneuropathy with endoneurial immune complex deposition as the first manifestation of systemic lupus erythematosus

1998 ◽  
Vol 96 (3) ◽  
pp. 297-300 ◽  
Author(s):  
I. Bódi ◽  
P. Váradi ◽  
G. Pokorny ◽  
J. Engelhardt ◽  
G. Dibó ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Immune Complex ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Immune Complex Deposition ◽  
Complex Deposition
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