Immune complex formation

There are also other immimological mechanisms, especially via IgG or IgM antibodies with immune complex formation, which can lead to similar clinical conditions [20, 34, 42] as has been shown in dextran anaphylaxis (table 1). Triggering of mast cells and basophils leads to release of various vasoactive mediators, among which histamine was the first recognized in 1908 (fig. 3,4) [6]. 

Episodic or chronic arthritis and hypertrophic pulmonary osteoarthropathy may also occur due to immune complex formation in response to chronic inflammation.11 Digital clubbing is commonly observed and is a marker for hypoxia. 

In summary, the in vivo protective effects of Tyv-specific antibodies, exclusion and immobility, can now be effectively studied using an in vitro model of the intestinal epithelium. Larvae are prevented from entering epithelial cells by caps of immune complexes or by binding of antibody to Tyv in the absence of immune complex formation. These effects would correlate with exclusion of larvae from epitheha observed in passively immunized rats. Larvae are encumbered as they migrate within epithelial monolayers, an effect that may correlate with immobility of larvae observed in vivo. It is reasonable to conclude that in the animal host the different effects work in combination, most iikeiy in cooperation with innate host defences, to cause nematode expuision from the intestine. 

Mechanisms underlying non-IgE mediated food allergy include immune complex formation and activation of lymphocytes. As with IgE-mediated responses, manifestations can be in the skin, gut, or respiratory tract however, these reactions take several hours to days to develop [65],... 

In nearly all cases studied, the amount of primary antibody required in the E5-Ab complex to perform an assay has been found to be substantially less than that required for the double antibody immune complex format. This was found to be the case (Table 19.1) when the E5-Ab complex was either directly immobilized on the solid phase, to imitate the double-antibody immune complex format, or utilized in a solution phase format [12],... 

One of the approaches is to use colloidal gold as label [29] in electrochemical immunoassay. In addition to standard stages of the immune complex formation, oxidative release of gold and removal of excessive bromine are included into the analysis procedure. 

Fig. 27.2. Immune complex formation and its reaction with silver label.

We are also trying a new drug for SLE patients. Cordyceps sinensis (CS) is a traditional Chinese medicine with immunomodulatory effect. We have shown that MRL Ipr/lpr mice treated daily with HI-A extract of CS for 8 weeks show progressivly reduced anti-dsDNA production (Y3). Although there was no change in immune complex formation, there were less mesangial proliferation (Y3). 

Schmiedeke, T. M., Stockl, F. W., Weber, R., Sugisaki, Y., Batsford, S. R., and Vogt, A., Histones have high affinity for the glomerular basement membrane. Relevance for immune complex formation in lupus nephritis. J. Exp. Med. 169,1879—1894 (1989). 

Schematic of immune complex formation, elimination, and deposition.

Fab (50 kd) and scFv (27 kd) antibody fragments have shorter plasma half-lives (0.5 to 21 hours) because of more rapid glomerular filtration and clearance [7], Plasma clearance, particularly of the xenogenic (usually mouse) portions of humanized and/or chimeric monoclonal antibodies, might be accelerated by development of anti-mouse (or other species), anti-isotypic, anti-idiotypic, or anti-allotypic antibodies that foster immune complex formation or reticuloendothelial clearance via several different FcR forms or elicit allergic or anaphylactic responses [7,8]. 

In an extension study in 225 children there were no anaphylactic reactions or adverse events suggestive of serum sickness or immune complex formation anti-omalizumab antibodies were not detected (9). In cases of re-treatment there were no severe adverse events related to omalizumab (10). 

The previously discussed methods rely on evaluating the immune complex formation as an index of antigen antibody reaction. As demonstrated previously in equation (1), the overall reaction occurs in sequential phases, and only the final phase is the formation of the immune complex. However, the initial binding of the antibody and antigen has also been demonstrated to be very useful analytically and has been used with labeled antigens and antibodies to develop many sensitive and specific immunochemical assays. The reaction describing this initial binding and the kinetic constant for the overall reaction are shown in equations (4a) and (4b), respectively ... 

Immune dysregulation leading to B-cell hyperactivity and subsequent production of pathogenic autoantibodies, coupled with defective clearance of apoptotic cells, followed by immune-complex formation, complement activation, and defective clearance of immune complexes all lead to inflammatory reactions that ultimately result in tissue injury and damage. An overview of the pathogenesis of SLE is illustrated in Fig. 85-1. 

Platelet aggregation may occur as a result of immune-complex formation, resulting in the formation of microthrombi and the release of vasoactive mediators. Also, insoluble complexes may be phagocy-tized by macrophages and activate these cells. 

The immunoglobulins have been extensively studied by ITP (in serum and csf see Section 2.4.4) and in particular the subclasses of IgG have been studied (H8, HIO, Hll, Z3). An extension of this work has been the demonstration of soluble immune complex formation in vitro (H9), which has obvious implications, particularly for the assessment of immune complex diseases. Preparative work has involved the isolation of, for example, antibodies to pig lactate dehydrogenase (B21, PI) and IgD myeloma protein (Jl). ITP has also been applied in the field of en-zymology, not for the direct measurement of enzymes as proteins, but for the determination of enzyme reaction substrates and products, and hence has been of use in enzyme kinetics. This work is summarized in Table 1. 

III. Immune complex formation-vasculitis, serum sickness, interstitial nephritis... 

The mechanism of action of the immunological and anti-inflammatory effects of antimalarials include inhibition of phospholipase A, inhibition of platelet aggregation, a range of lysosomal effects (e.g., an increase in pH, membrane stabilization, and inhibition of release and activity of lysosomal enzymes), inhibition of phagocytosis, an increase in intracellular pH in cytoplasmic vacuoles leading to decreased stimulation of autoimmune CD4 T cells, decreased cytokine release from lymphocytes and stimulated monocytes, inhibition of immune complex formation, and antioxidant activity. In patients with porphyria cutanea tarda, chloroquine and hydroxychloroquine bind to porphyrins and/or iron to facilitate their hepatic clearance. The ability to bind to melanin and other pigments may contribute to the retinal toxicity seen occasionally when anti-malarial agents are used. 

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