Recombinant soluble human Fc gamma RII: production, characterization, and inhibition of the Arthus reaction.

Ierino, Frank; Powell, Maree S.; McKenzie, Ian F. C.; Hogarth, P. Mark

doi:10.1084/jem.178.5.1617

Cited by 87 publications

(45 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our results suggest that CD32A-Ig is not able to compete with mouse Fc␥Rs for binding to IC either because the affinity of CD32A-Ig may be too low, or mouse Fc␥Rs and human CD32A may be binding to distinct regions of rabbit IgG. Thus our results, although supporting the observation reported by Ireino et al 52 that CD32A cannot practically block the IC-mediated inflammation, do, however, demonstrate the feasibility of using systemic administration of CD16A-Ig to block acute inflammation mediated by IC.…”

Section: Fc␥r Dimers Block Neutrophil Emigration 901contrasting

confidence: 56%

“…18,46,51 In contrast to our observations with recombinant soluble CD16A-Ig dimer presented here, an earlier study that used a recombinant soluble CD32A has concluded that parenterally administered soluble Fc␥Rs is not a practical approach to block IC-mediated inflammation. 52 Their conclusion was based on the observation that the systemically administered CD32A has a half-life of only 25 minutes and is unable to block Arthus reaction. This report also showed that soluble CD32A could block Arthus reaction only when administered locally along with the IC at a concentration of 5mg/mL.…”

Section: Fc␥r Dimers Block Neutrophil Emigration 901mentioning

confidence: 99%

See 1 more Smart Citation

Extravasations and emigration of neutrophils to the inflammatory site depend on the interaction of immune-complex with Fcγ receptors and can be effectively blocked by decoy Fcγ receptors

Shashidharamurthy

Hennigar

Fuchs

et al. 2008

Blood

View full text Add to dashboard Cite

IntroductionAutoimmune diseases are heterogeneous in nature and are the most frequent cause of disability in adults. 1 Many autoimmune diseases lead to vital organ damage, disability and are often fatal in humans. Both the cellular and humoral arms of the immune system are involved in the pathogenesis of autoimmune diseases. Abnormal activation of autoantigen specific T and B cells due to molecular mimicry, viral infections, or cytokine dysregulation are among the suggested mechanisms for the initiation of the disease. 2 In many autoimmune diseases the binding of autoantibodies to tissues causes tissue injury. The effector functions of the Fc domains of these tissue-antigen bound antibodies depend on their ability to interact with complement components and/or Fc gamma receptors (Fc␥Rs) expressed on inflammatory cells. The relative role and contribution of these 2 effector systems to the initiation and development of antibody mediated inflammatory diseases are still under intense investigation.Studies have shown that the accumulation of neutrophils at the site of IC deposition is pivotal to the development of antibodymediated autoimmune inflammation. 3 The ICs trigger complement activation and production of chemotactic peptides such as C5a, which directly attract neutrophils to the inflammatory site. 4,5 Apart from attracting neutrophils, C5a also induce degranulation of mast cells resulting in further recruitment of neutrophils to the site of IC deposition. [5][6][7] These studies were further supported by the fact that mice deficient in C5a receptor gene show attenuated autoantibodyinduced inflammation. 4,8 Thus the complement peptides produced by IC orchestrate accumulation of neutrophils and cause tissue damage. On the other hand, studies using Fc␥ knockout mice have demonstrated the pivotal role of Fc␥Rs in neutrophil recruitment 9,10 and antibody-mediated autoimmune diseases. The Fc␥ subunit is essential for cell-surface expression of activating Fc␥Rs such as CD64, Fc␥RIV, and CD16A. [11][12][13][14] These Fc␥ or CD16A gene knockout mice did not develop autoimmune diseases under experimental conditions that induced the diseases in wild type mice. [15][16][17][18] Although these knockout mice studies have demonstrated independent roles of complement and Fc␥Rs, recent observations suggest interdependency of these 2 pathways in the progression of inflammation. 19 At the inflammatory site, C5a increases the potency of the Fc␥R-dependent inflammatory pathway by up-regulating activating CD16A while downregulating inhibitory CD32B in inflammatory cells. 20 Furthermore, the interaction of IC with CD16A upregulates the production of cell-derived C5. 21 This suggests that the absence of the complement pathway might influence the effectiveness of the Fc␥R-mediated pathway of inflammation and vice versa. Because many of these studies used either gene knockout mice or mast cell deficient mice which might have adapted developmental compensatory mechanisms, the results and interpretations of the relative role of these fun...

show abstract

Section: Fc␥r Dimers Block Neutrophil Emigration 901contrasting

confidence: 56%

Section: Fc␥r Dimers Block Neutrophil Emigration 901mentioning

confidence: 99%

Extravasations and emigration of neutrophils to the inflammatory site depend on the interaction of immune-complex with Fcγ receptors and can be effectively blocked by decoy Fcγ receptors

Shashidharamurthy

Hennigar

Fuchs

et al. 2008

Blood

View full text Add to dashboard Cite

show abstract

“…However, more recent studies have suggested that IC-mediated inflammation in the RPA reaction is initiated via Fc␥ receptor-triggered pathways. For example, treatment of rats with recombinant soluble human Fc␥RII was shown to lead to a dose-dependent inhibition of the RPA response (5), and targeted deletion of the FcR ␥-chain resulted in markedly attenuated RPA reactions in mice (6,7). In addition, it was reported that in mice deficient in complement proteins C3, C4, or C5 the RPA reaction develops normally (8).…”

mentioning

confidence: 99%

The Arthus Reaction in Rodents: Species-Specific Requirement of Complement

Szalai

Digerness²,

Agrawal

et al. 2000

The Journal of Immunology

View full text Add to dashboard Cite

We induced reverse passive Arthus (RPA) reactions in the skin of rodents and found that the contribution of complement to immune complex-mediated inflammation is species specific. Complement was found to be necessary in rats and guinea pigs but not in C57BL/6J mice. In rats, within 4 h after initiation of an RPA reaction, serum alternative pathway hemolytic titers decreased significantly below basal levels, whereas classical pathway titers were unchanged. Thus the dermal reaction proceeds coincident with systemic activation of complement. The serine protease inhibitor BCX 1470, which blocks the esterolytic and hemolytic activities of the complement enzymes Cls and factor D in vitro, also blocked development of RPA-induced edema in the rat. These data support the proposal that complement-mediated processes are of major importance in the Arthus reaction in rats and guinea pigs, and suggest that BCX 1470 will be useful as an anti-inflammatory agent in diseases where complement activation is known to be detrimental.

show abstract

“…Recent therapeutic approaches to the Arthus reaction focus on the use of recombinant soluble human complement receptor type I (Rossi et al, 1992) to control the activation of the complement cascade, the utilization of a recombinant soluble form of human Fc-yRII (Fc-yR, receptor for the Fc portion of IgG) genetically engineered to interfere with neutrophil activation via Fc-yRII, and the ensuing release of inflammatory mediators (Ierino et al, 1993); and the utilization of recombinant selectin chimeric molecules to block PMN recruitment (Mulligan et al, 1993). Another step for pharmacological modulation might be the antagonism of mediators released from PMN that could be particularly active either on their own or because of their central position Brfth Journal of Pharmacology (1995) 114.…”

Section: Introductionmentioning

confidence: 99%

Platelet‐activating factor: the effector of protein‐rich plasma extravasation and nitric oxide synthase induction in rat immune complex peritonitis

Steil¹,

Garcia‐Rodriguez²,

Crespo³

1995

British J Pharmacology

View full text Add to dashboard Cite

1 The involvement of platelet-activating factor (PAF) in immune complex-induced/polymorphonuclearmediated tissue injury was studied by use of a reverse passive Arthus (RPA) model in the peritoneal cavity of rats. 2 Extravasation of protein-rich plasma, accumulation of polymorphonuclear leukocytes (PMN), and the production of nitric oxide (NO) by resident peritoneal mononuclear phagocytes were assayed. 3 Treatment of rats with either UR-12460 or BB-823, two compounds which possess different chemical structures, but elicit the same antagonistic effect on the PAF receptor, abrogated protein-rich plasma extravasation. In contrast, they did not show any effect on the accumulation of PMN. 4 Inhibition of NO production with both N1-mono methyl-L-arginine and N0-nitro-L-arginine failed to prevent protein-rich plasma extravasation. 5 The production of NO by peritoneal adherent cells following RPA was measured in cells maintained for 2 to 28 h in culture, and it was significantly increased in cells removed as early as 15 min after RPA induction, as compared to controls. 6 Addition of 10 nM PAF to the culture medium reduced the generation of NO by peritoneal cells from RPA rats, whereas this mediator enhanced NO production in cells from naive control animals. 7 Treatment with either UR-12460 or BB-823 prior to the induction of RPA produced an almost complete inhibition of NO production. 8 Assay of nitric oxide synthase activity in cell homogenates from peritoneal cells showed that the activity was due to the inducible form of the enzyme. 9 Study by Northen blotting of mRNA coding for the inducible NO synthase (iNOS) showed transcription at 6 and 18 h after the induction of RPA, which was inhibited in UR-12460-treated rats. 10 These data indicate that PAF is the main mediator of the early plasma leakage observed in RPA, and also that PAF is implicated in the triggering of long-term changes via induction of specific genes, as judged from its ability to promote the expression of iNOS.

show abstract

Recombinant soluble human Fc gamma RII: production, characterization, and inhibition of the Arthus reaction.

Cited by 87 publications

References 67 publications

Extravasations and emigration of neutrophils to the inflammatory site depend on the interaction of immune-complex with Fcγ receptors and can be effectively blocked by decoy Fcγ receptors

Extravasations and emigration of neutrophils to the inflammatory site depend on the interaction of immune-complex with Fcγ receptors and can be effectively blocked by decoy Fcγ receptors

The Arthus Reaction in Rodents: Species-Specific Requirement of Complement

Platelet‐activating factor: the effector of protein‐rich plasma extravasation and nitric oxide synthase induction in rat immune complex peritonitis

Contact Info

Product

Resources

About