Plasma Exchange and Immune Complex Diseases:
The Predictability of Immune Complexes Removal to
Clinical Response

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).

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Plasma Exchange as a Therapy for Guillain-Barré Syndrome with Immune Complexes

Vox Sanguinis ◽

10.1111/j.1423-0410.1981.tb01017.x ◽

1981 ◽

Vol 41 (2) ◽

pp. 74-78 ◽

Cited By ~ 33

Author(s):

M. Valbonesi ◽

S. Garelli ◽

L. Mosconi ◽

D. Zerbi ◽

I. Celano

Keyword(s):

Plasma Exchange ◽

Immune Complexes ◽

Guillain Barre Syndrome ◽

Guillain Barré Syndrome ◽

Guillain Barré

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Changes in coagulation factors, complement, immunoglobulins, and immune complex concentrations with plasma exchange

Transfusion ◽

10.1046/j.1537-2995.1982.22182154218.x ◽

1982 ◽

Vol 22 (1) ◽

pp. 54-58 ◽

Cited By ~ 34

Author(s):

RL Volkin ◽

TW Starz ◽

A Winkelstein ◽

RK Shadduck ◽

JH Lewis ◽

...

Keyword(s):

Plasma Exchange ◽

Immune Complex ◽

Coagulation Factors

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Neutrophil-mediated cellular cytotoxicity triggered by immobilized aggregated IgG: Anin vitro model of cell injury during immune complex diseases

Journal of Clinical Immunology ◽

10.1007/bf00916573 ◽

1984 ◽

Vol 4 (6) ◽

pp. 439-444 ◽

Cited By ~ 1

Author(s):

Franco Dallegri ◽

Franco Patrone ◽

Guido Frumento ◽

Alberto Ballestrero ◽

Carlo Sacchetti

Keyword(s):

Immune Complex ◽

Cell Injury ◽

Complex Diseases ◽

Cellular Cytotoxicity ◽

Vitro Model

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Dexamethasone-Induced Apoptosis of Human Monocytes Exposed to Immune Complexes. Intervention of CD95-and Xiap-Dependent Pathways

International Journal of Immunopathology and Pharmacology ◽

10.1177/039463200501800302 ◽

2005 ◽

Vol 18 (3) ◽

pp. 403-415 ◽

Cited By ~ 18

Author(s):

L. Ottonello ◽

M. Bertolotto ◽

F. Montecucco ◽

P. Dapino ◽

F. Dallegri

Keyword(s):

Immune Complex ◽

Immune Complexes ◽

Therapeutic Option ◽

Mek Inhibitor ◽

Dependent Manner ◽

Human Monocytes ◽

Inflammatory Reactions ◽

Activated Monocytes ◽

Induced Apoptosis ◽

Dose Dependent

Monocytes and macrophages play a key role in the initiation and persistence of inflammatory reactions. The possibility to interfere with the survival of these cells, once recruited and activated at sites of inflammation, is an attractive therapeutic option. Although resting monocytes are susceptible to pharmacologically induced apoptosis, no data are available about the possibility to modulate the survival of activated monocytes. The present work was planned to investigate if dexamethasone is able to promote apoptosis of human monocytes activated by immune complexes. When monocytes were cultured with immune complexes, a dose-dependent inhibition of apoptosis was observed. Dexamethasone stimulated apoptosis of resting and activated monocytes in a dose-dependent manner. Both the immune complex inhibitory activity and dexamethasone stimulatory properties depend on NF-kB/XIAP and Ras/MEK/ERK/CD95 pathways. In fact, the exposure of monocytes to immune complexes increased NF-kB activation and XIAP expression, which in turn were inhibited by dexamethasone. On the other hand, immune complex-stimulated monocytes displayed a reduced expression of CD95, which is prevented by dexamethasone, as well as by MEK inhibitor U0126. Furthermore, anti-CD95 ZB4 mAb prevented dexamethasone-induced apoptosis in immune complex-stimulated monocytes. Similarly, ZB4 inhibited dexamethasone-mediated augmentation of caspase 3 activity. The present findings suggest that Fc triggering by insoluble immune complexes result in the activation of two intracellular pathways crucial for the survival of monocytes: 1. Ras/MEK/ERK pathway responsible for the down-regulation of CD95 expression; 2. NF-kB pathway governing the expression of XIAP. Both the pathways are susceptible to inhibition by monocyte treatment with pharmacologic concentrations of dexamethasone.

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Protein kinase activities in immune complexes of simian virus 40 large T-antigen and transformation-associated cellular p53 protein

Molecular and Cellular Biology ◽

10.1128/mcb.4.2.232-239.1984 ◽

1984 ◽

Vol 4 (2) ◽

pp. 232-239

Author(s):

F Van Roy ◽

L Fransen ◽

W Fiers

Keyword(s):

Monoclonal Antibodies ◽

Immune Complex ◽

Immune Complexes ◽

Kinase Activity ◽

P53 Protein ◽

Simian Virus 40 ◽

Simian Virus ◽

T Antigen ◽

Large T Antigen

Immune complex kinase assays in the simian virus 40 system were performed by incubation of immunoprecipitates containing tumor antigens with [gamma-32P]ATP, followed by analysis of any phosphoacceptor proteins. These assays yielded mainly the viral large T-antigen and, in particular, the associated cellular p53 as endogenous substrates. The nature of these substrates was confirmed by proteolysis techniques. Under specific conditions, casein could be used as an exogenous substrate as well. The kinase reactions showed preference for ATP and MgCl2 instead of GTP or MnCl2. Both phosphoserine and phosphothreonine, but in no case phosphotyrosine, were detected after an immune complex kinase reaction. Apparently, several in vivo phosphorylation sites were recognized in vitro in both large T-antigen and p53, but the presence of some artifactual sites could not be completely excluded. Although contaminating kinases were detectable in the immune complexes, at least the p53 molecules were phosphorylated in vitro in a more specific way. This followed from several characteristics of the immune complex kinase reactions and especially from the strong inhibition of p53 phosphorylation by two anti-large-T monoclonal antibodies. It was shown that large T-antigen showed associated kinase activity, although none of our results could unambiguously demonstrate an intrinsic kinase activity of this protein. Finally, anti-p53 monoclonal antibodies only slightly affected in vitro phosphorylation reactions, whereas a p53 molecule from a simian virus 40-free, chemically transformed human cell line was not phosphorylated in vitro under any condition tested. Thus, it is highly unlikely that the p53 molecule per se carries intrinsic or even associated kinase activities.

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

Clinical Chemistry ◽

10.1093/clinchem/28.6.1259 ◽

1982 ◽

Vol 28 (6) ◽

pp. 1259-1271 ◽

Cited By ~ 25

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.

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