Localization of Immune Complexes in the Basement Membrane of the Ductuli Efferentes of the Rhesus Monkey

1980 ◽  
Vol 38 ◽  
pp. 456-457
Author(s):  
D. Marsh
Keyword(s):  
Basement Membrane ◽  
Fluorescence Microscopy ◽  
Rhesus Monkey ◽  
Immune Complex ◽  
Immune Complexes ◽  
Vas Deferens ◽  
Frozen Sections ◽  
Efferent Ducts ◽  
Complex Deposition ◽  
Sperm Antibodies

As a result of vasectomy, spermatozoa are confined to the epididymis and vas deferens, where they degenerate, releasing antigens that enter the circulation or are engulfed by macrophages. Multiple antigens of the sperm can elicit production of autoantibodies; circulating anti-sperm antibodies are found in a large percentage of vasectomized men, indicating the immunogenicity of the sperm. The increased prevalence of macrophages in the liomen of the rhesus monkey testicular efferent ducts after vasectomy led to further study of this region. Frozen sections were used for evaluation of immunopathological status by fluorescence microscopy with fluorescein-conjugated antibody. Subsequent granular deposits of immune complexes were revealed by positive immunofluorescence staining for complement. The immune complex deposition in the basement membrane surrounding the efferent ducts implies that this region is involved in antigen leakage (Fig. 1).

scholarly journals Localization of the membrane attack complex (MAC) in experimental immune complex glomerulonephritis.

1983 ◽  
Vol 157 (6) ◽  
pp. 1885-1905 ◽  
Author(s):  
D Koffler ◽  
G Biesecker ◽  
B Noble ◽  
G A Andres ◽  
A Martinez-Hernandez
Keyword(s):  
Basement Membrane ◽  
Immune Complex ◽  
Immune Complexes ◽  
Tissue Injury ◽  
Membrane Attack Complex ◽  
Intense Staining ◽  
Immune Complex Glomerulonephritis ◽  
Filtration Barrier ◽  
Dense Deposits ◽  
Foot Process

The role of the membrane attack complex (MAC) as a mediator of renal tissue injury was evaluated in rats affected by bovine serum albumin (BSA)-induced immune complex glomerulonephritis. Immunofluorescence studies revealed concurrent deposits of IgG, BSA, C3, and the MAC along glomerular capillary walls, although the MAC manifested a more restricted distribution than that observed for immune complexes. Immunoelectron microscopic techniques were utilized to demonstrate immune complexes, C3, and the MAC within dense deposits in the subepithelial aspect of the basement membrane. Visceral epithelial foot processes were fused in areas overlying large dense deposits and exhibited intense staining for the MAC, lesser reactivity for C3 but IgG was absent from the foot process membranes. Smaller granular deposits of immune complexes, C3, and the MAC were observed in the subendothelial region of the lamina rara interna and the lamina densa. Immune complexes may activate the classical complement pathway causing diffuse injury to the glomerular basement membrane (GBM), allowing subepithelial accumulation of complexes. These observations implicate the MAC as a mediator of GBM and juxtaposed podocyte membrane injury, thereby contributing to disruption of the glomerular filtration barrier. IgG and C3 were demonstrated within tubulointerstitial regions on the surface of collagen fibers in close proximity to the tubular basement membrane (TBM) of proximal convoluted tubules. Within the TBM, C3 localization was prominent with diminished reactivity for the MAC, but IgG was not detectable. The demonstration of C3 and scant MAC deposits in the TBM of nonimmunized control rats without evidence of interstitial IgG and C3 deposits suggests that both nonimmune and immune processes play a role in the pathogenesis of extraglomerular lesions. Evidence derived from these morphologic studies indicates that the MAC is associated with injury to the GBM, foot process membranes of visceral epithelium, and the TBM. Further experiments designed to selectively enhance or inhibit the deposition of MAC and assess consequent renal dysfunction are required to substantiate hypotheses concerning the in vivo membranolytic potential of the MAC in experimental immune complex glomerulonephritis.

INTERACTION OF CELLS WITH IMMUNE COMPLEXES: ADHERENCE, RELEASE OF CONSTITUENTS, AND TISSUE INJURY

1971 ◽  
Vol 134 (3) ◽  
pp. 114-135 ◽  
Author(s):  
Peter M. Henson
Keyword(s):  
Electron Microscope ◽  
Immune Complex ◽  
Immune Complexes ◽  
Tissue Damage ◽  
Tissue Injury ◽  
Surrounding Medium ◽  
The Body ◽  
Joint Fluid ◽  
Complex Deposition

Neutrophils are essential mediators of tissue damage in many forms of immune complex-induced injury. In vitro, they have been shown to release some of their content of injurious constituents upon reaction with immune complexes (Fig. 10). If the complexes are distributed along a nonphagocytosable surface, degranulation to the exterior of the cell is observed. When the complexes were phagocytized, however, degranulation into the phagocytic vacuole, and some loss of enzymes into the surrounding medium, occurred. This may have resulted from a momentary opening of the vacuole to allow ingestion of additional particles, as was demonstrated with the electron microscope. This phenomenon was particularly noticeable when the particles were relatively large. Far more immune complex is required to induce release when in a phagocytosable form than when on a nonphagocytosable membrane. Neutrophils may be attracted to sites of immune complex deposition in many parts of the body (arteries, heart, skin, brain, kidney, joints) by complement-mediated processes. In some situations, e.g. in the joint fluid, they would encounter free immune complexes, phagocytose them, and release enzymes. In many others, in which immune complexes may be distributed along surfaces, such as in the glomerulus, adherence of neutrophils may also lead to release of injurious constituents (proteases, collagenase, elastase, permeability factors) capable of digesting and injuring the tissues.

scholarly journals INTERSTITIAL IMMUNE COMPLEX THYROIDITIS IN MICE

1974 ◽  
Vol 140 (6) ◽  
pp. 1439-1456 ◽  
Author(s):  
James A. Clagett ◽  
Curtis B. Wilson ◽  
William O. Weigle
Keyword(s):  
Basement Membrane ◽  
Immune Complex ◽  
Immune Complexes ◽  
Basal Area ◽  
Dense Deposits ◽  
Thyroid Glands ◽  
Intimate Association ◽  
In Situ Formation ◽  
Neutrophil Infiltrate

Mice immunized with soluble heterologous thyroglobulins developed autoantibody that cross-reacted with autologous thyroglobulin. There was a direct correlation between the temporal appearance and quantity of serum autoantibody and the presumed in situ formation of immune complexes in the interstitium of the thyroid glands. Immediately after the formation of interstitial immune complexes containing antibody of the IgG complement-fixing type, the thyroids were invaded by a transient but intense neutrophil infiltrate which within 1 wk was replaced by chronic mononuclear elements. By the combination of fluorescence microscopy and autoradiography, thyroglobulin was demonstrated to be one, if not the sole, antigen in the interstitial immune complexes. The interstitial immune complexes were granular to lumpy in appearance and formed at the basal area of the follicular cells in intimate association with the follicular basement membrane. Electron microscopy revealed electron dense deposits, presumably immune complexes, between the follicular basement membrane and the plasma membrane. The presumed in situ formation of immune complexes in this model is similar to that which occurs in the Arthus reaction and is a different mechanism of immune complex injury than that caused by tissue deposition of circulating immune complexes as occurs in serum sickness.

scholarly journals Enhancement of glomerular immune complex deposition by a circulating polycation.

1984 ◽  
Vol 160 (1) ◽  
pp. 286-293 ◽  
Author(s):  
J L Barnes ◽  
M A Venkatachalam
Keyword(s):  
Electron Microscopy ◽  
Bovine Serum Albumin ◽  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Immune Complexes ◽  
Glomerular Polyanion ◽  
Quantitative Immunofluorescence ◽  
Complex Deposition ◽  
Capillary Walls ◽  
Made In

It is known that polycations bind to and neutralize glomerular polyanions. Here we examine the effect of the polycation polyethyleneimine (PEI) on glomerular deposition of preformed immune complexes. Bovine serum albumin (BSA)-anti-BSA immune complexes made in 40 times antigen excess were administered following intravenous injection of PEI. Glomerular localization of immune deposits was assessed by quantitative immunofluorescence and electron microscopy and compared to controls receiving diluent without PEI followed by the same dose in immune complexes. In rats receiving PEI, deposits were localized within the glomerular basement membrane (GBM) of all peripheral capillary walls and in the mesangium. In controls, deposits localized exclusively within the mesangium in smaller amounts than after PEI. Thus, neutralization of glomerular polyanion by a circulating polycation enhances the deposition and alters the distribution of immune complexes in glomeruli.

scholarly journals Levamisole/Cocaine Induced Systemic Vasculitis and Immune Complex Glomerulonephritis

2015 ◽  
Vol 2015 ◽  
pp. 1-5 ◽  
Author(s):  
Lohit Garg ◽  
Sagar Gupta ◽  
Abhishek Swami ◽  
Ping Zhang
Keyword(s):  
Immune Complex ◽  
Systemic Vasculitis ◽  
Renal Involvement ◽  
Morphological Properties ◽  
High Dose ◽  
Cocaine Use ◽  
Immune Mediated ◽  
History Of ◽  
Psychotropic Effects ◽  
Complex Deposition

Levamisole is an antihelminthic and immunomodulator medication that was banned by the USFDA in 1998. It has been increasingly used to adulterate cocaine due to its psychotropic effects and morphological properties. Adverse reactions including cutaneous vasculitis, thrombocytopenia, and agranulocytosis have been well described. Despite systemic vasculitis in this setting, renal involvement is uncommon. We report here a case of ANCA positive systemic vasculitis with biopsy proven immune complex mediated glomerulonephritis likely secondary to levamisole/cocaine. A 40-year-old Caucasian male with no past medical history presented with 3-week history of fatigue, skin rash, joint pains, painful oral lesions, oliguria, hematuria, worsening dyspnea on exertion, and progressive lower extremity edema. He had a history of regular tobacco and cocaine use. Lab testing revealed severe anemia, marked azotemia, deranged electrolytes, and 4.7 gm proteinuria. Rheumatologic testing revealed hypocomplementemia, borderline ANA, myeloperoxidase antibody, and positive atypical p-ANCA. Infectious and other autoimmune workup was negative. Kidney biopsy was consistent with immune mediated glomerulonephritis and showed mesangial proliferation and immune complex deposition consisting of IgG, IgM, and complement. High dose corticosteroids and discontinuing cocaine use resulted in marked improvement in rash, mucocutaneous lesions, and arthritis. There was no renal recovery and he remained hemodialysis dependent.

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.

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