In vitro production of interleukin‐1 receptor antagonist in IgG‐ mediated red cell incompatibility

Davenport, R. D.; Burdick, Marie D.; Strieter, Robert M.; Kunkel, S L

doi:10.1046/j.1537-2995.1994.34494233576.x

Cited by 24 publications

(8 citation statements)

References 49 publications

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“…Earlier reports have demonstrated that intravenous immunoglobulin can significantly increase IL1ra levels in vivo, 28,29 and Davenport et al 30 also showed that anti-D-coated RBCs could stimulate peripheral blood mononuclear cells (PBMCs) in vitro to secrete IL1ra within 4 hours. The researchers suggested that anti-D-induced cytokine alterations might account for some of the pathophysiologic events seen in IgG-mediated immune hemolysis.…”

Section: Discussionmentioning

confidence: 98%

Anti-D initially stimulates an Fc-dependent leukocyte oxidative burst and subsequently suppresses erythrophagocytosis via interleukin-1 receptor antagonist

Coopamah

Freedman

Semple

2003

Blood

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Section: Discussionmentioning

confidence: 98%

Anti-D initially stimulates an Fc-dependent leukocyte oxidative burst and subsequently suppresses erythrophagocytosis via interleukin-1 receptor antagonist

Coopamah

Freedman

Semple

2003

Blood

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“…PBMCs from AIHA patients would be predicted to secrete a wide variety of cytokines when stimulated with RBC antigens, 41,42 and those measured here were selected to be characteristic of particular CD4 ϩ Th subsets. The RhD protein was chosen as the autoantigen studied, since Th cells specific for epitopes from this protein are activated in AIHA patients with autoantibodies specific for the Rh complex, 29 and it affords a unique comparison with alloimmune responses in RhD-negative healthy control donors who had been deliberately immunized with RhD-positive RBCs.…”

Section: Discussionmentioning

confidence: 99%

Interleukin-10–mediated regulatory T-cell responses to epitopes on a human red blood cell autoantigen

Hall

Ward

Vickers

et al. 2002

Blood

110

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“…[33][34][35] Therefore, we found it relevant to establish the role of EndoS regarding the in vitro response of monocytes exposed to sensitized RBCs by measuring the release of IL-8. Thus, THP-1 cells and monocytes were incubated with anti-D-sensitized RBCs, and the secretion of IL-8 was measured using ELISA.…”

Section: Endos Inhibits Il-8 Secretion From Monocytes Induced By Sensmentioning

confidence: 99%

The IgG-specific endoglycosidase EndoS inhibits both cellular and complement-mediated autoimmune hemolysis

Maria

Briceno

Baudino

et al. 2010

Blood

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EndoS from IntroductionThe presence and pathogenicity of autoantibodies directed against red blood cells (RBCs) have been extensively investigated and implicated in a number of autoimmune diseases, such as autoimmune hemolytic anemia (AIHA) 1 and systemic lupus erythematosus. 2 The RBC surface contains many epitopes recognizable by alloantibodies and autoantibodies, including the more than 300 blood group antigens located on glycoproteins and glycolipids but also nonpolymorphic/nonblood group protein structures. 3 The most common targets of pathogenic RBC autoantibodies are epitopes on the Rh protein, encoded by 2 homologous genes on chromosome 1, RHD and RHCE. 4 More than half of all autoantibody specificities in patients with AIHA of the common so-called warm type include immunoglobulin G (IgG) antibodies against these Rh epitopes, which are consequently often used to model AIHA experimentally.Human antibodies against RhD (anti-D) or rabbit antibodies against human RBC (anti-RBC) can result in accelerated phagocytosis and removal of RBC from the circulation by monocytes/ macrophages in the spleen and liver. 5,6 Fc␥ receptor (Fc␥R)-mediated erythrophagocytosis, in addition to other IgG effector functions, such as activated complement, oxidative burst, and cytokine production by Fc␥R expressing effectors cells, play an essential role in shortened RBC survival. [7][8][9][10][11] The ability of normal human monocytes to bind and phagocyte IgG-sensitized RBCs via Fc␥R and mediate immune RBC destruction is highly related to the glycosylation status of the Fc domain on the anti-RBC antibodies. [12][13][14][15][16][17] Endoglycosidase S (EndoS) is secreted by Streptococcus pyogenes and has a specific endoglycosidase activity on native IgG by hydrolyzing the conserved asparagine-linked glycans on the heavy chains of IgG. 18,19 EndoS is the first known bacterial enzyme with a unique specificity for native IgG. EndoS affects the functionality of opsonizing IgG by decreased binding to Fc␥Rs on a monocyte-like cell line and impaired classic complement activation in vitro. 19 EndoS has recently been shown to modulate human IgG/Fc␥R interactions by influencing the binding/dissociation of IgG to soluble and cell-bound Fc␥R. 20 Furthermore, the pretreatment of pathogenic antibodies by EndoS has a protective function in a mouse model of collagen-induced arthritis, and EndoS cures mice from lethal IgG-driven immune thrombocytopenic purpura (ITP). 21,22 The present study was undertaken to establish the effects of EndoS on antibody-mediated destruction of RBCs with a future therapeutic application in mind. Here we show, using monocytes from blood and the THP-1 monocytic cell line, that pretreatment of anti-RBC with EndoS abrogates erythrophagocytosis and subsequent activation of monocytes. The complement-dependent hemolytic effects of anti-RBC added to whole human blood were greatly decreased by pretreatment of this antibody with EndoS. Finally and most importantly, EndoS showed inhibitory effects on a model of AIHA in mice. These...

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In vitro production of interleukin‐1 receptor antagonist in IgG‐ mediated red cell incompatibility

Abstract: These results suggest that IL-1ra production may partly account for the variable pathophysiologic events seen in IgG-mediated autoimmune hemolysis and hemolytic transfusion reactions. Steroid treatment may also downregulate anti-inflammatory cytokine production in immune hemolysis.

Cited by 24 publications

References 49 publications

Anti-D initially stimulates an Fc-dependent leukocyte oxidative burst and subsequently suppresses erythrophagocytosis via interleukin-1 receptor antagonist

Anti-D initially stimulates an Fc-dependent leukocyte oxidative burst and subsequently suppresses erythrophagocytosis via interleukin-1 receptor antagonist

Interleukin-10–mediated regulatory T-cell responses to epitopes on a human red blood cell autoantigen

The IgG-specific endoglycosidase EndoS inhibits both cellular and complement-mediated autoimmune hemolysis

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