Studies on the Binding of Immunoglobulins and Immune Complexes to the Surface of Human Platelets: IgG Molecules React with Platelet Fc Receptors with the CH3 Domain

1982 ◽  
Vol 67 (1) ◽  
pp. 33-39 ◽  
Author(s):  
Gerhard K.M. Endresen ◽  
Øystein Førre
Keyword(s):  
Immune Complexes ◽  
Fc Receptors ◽  
Human Platelets

Immune complexes and IgG-Fc receptors on human platelets in essential mixed cryoglobulinemia

1986 ◽  
Vol 16 (2) ◽  
Author(s):  
Sebastiano Garelli ◽  
Pier Luigi Meroni ◽  
Giuseppina Musmanno ◽  
Wilma Barcellini ◽  
Fulvio Invernizzi
Keyword(s):  
Immune Complexes ◽  
Fc Receptors ◽  
Mixed Cryoglobulinemia ◽  
Human Platelets ◽  
Essential Mixed Cryoglobulinemia

scholarly journals Differential signal transduction, membrane trafficking, and immune effector functions mediated by FcγRI versus FcγRIIa

Blood ◽  
2009 ◽  
Vol 114 (2) ◽  
pp. 318-327 ◽  
Author(s):  
Xilei Dai ◽  
Manikandan Jayapal ◽  
Hwee Kee Tay ◽  
Renji Reghunathan ◽  
Gen Lin ◽  
...  
Keyword(s):  
Antigen Presentation ◽  
Mhc Class Ii ◽  
Membrane Trafficking ◽  
Immune Complexes ◽  
Antigen Processing ◽  
Fc Receptors ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Human Leukocyte ◽  
Differential Signal ◽  
Proinflammatory Mediators

Abstract Receptors for the fragment crystallizable region of immunoglobulin-G (FcγRs) play an important role in linking the humoral and cellular arms of the immune response. In this study, we present a comprehensive functional comparison of 2 human Fc-receptors, FcγRI and FcγRIIa. Activation of FcγRI results in a novel signaling cascade that links phospholipase D1 to sphingosine kinase-1 in U937 cells and primary human monocytes. This induces the expression of proinflammatory mediators and is associated with trafficking of immune complexes into human leukocyte antigen-DM positive antigen-processing compartments coupled with improved MHC class II–mediated antigen presentation to T lymphocytes. In contrast, activation of FcγRIIa elicits signaling through phospholipase Cγ1, resulting in increases in intracellular calcium, activation of nicotinamide adenine dinucleotide phosphate-oxidative burst, and differential membrane trafficking combined with impaired antigen presentation and proinflammatory cytokine expression. These data provide a mechanistic insight into the disparate activities associated with Fc receptors in immunity, namely, reinforcement of immune responses through stimulation of proinflammatory signaling and antigen presentation, versus the maintenance of immunologic homeostasis through the noninflammatory clearance of immune complexes.

scholarly journals Activation of human platelets by immune complexes prepared with cationized human IgG

Blood ◽  
1993 ◽  
Vol 82 (10) ◽  
pp. 3045-3051
Author(s):  
M Schattner ◽  
M Lazzari ◽  
AS Trevani ◽  
E Malchiodi ◽  
AC Kempfer ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activation ◽  
Immune Complexes ◽  
Platelet Rich Plasma ◽  
Human Platelets ◽  
Human Igg ◽  
Experimental Conditions ◽  
Induce Platelet Aggregation ◽  
Soluble Immune Complexes ◽  
High Concentrations

The present study shows that the ability of soluble immune complexes (IC), prepared with human IgG and rabbit IgG antibodies against human IgG, to trigger platelet activation was markedly higher for IC prepared with cationized human IgG (catIC) compared with those prepared with untreated human IgG (cIC). CatIC induced platelet aggregation and adenosine triphosphate release in washed platelets (WP), gel-filtered platelets (GFP), or platelet-rich plasma (PRP) at physiologic concentrations of platelets (3 x 10(8)/mL) and at low concentrations of catIC (1 to 30 micrograms/mL). On the contrary, under similar experimental conditions, cIC did not induce aggregation in PRP, WP, or GFP. Low aggregation responses were only observed using high concentrations of both WP (9 x 10(8)/mL) and cIC (500 micrograms/mL). Interestingly, catIC were also able to induce platelet activation under nonaggregating conditions, as evidenced by P-selectin expression. Cationized human IgG alone did not induce platelet aggregation in PRP but triggered either WP or GFP aggregation. However, the concentration needed to induce these responses, was about eightfold higher than those required for catIC. The responses induced either by catIC or cationized human IgG were completely inhibited by treatment with heparin, dextran sulphate, EDTA, prostaglandin E1, or IV3, a monoclonal antibody against the receptor II for the Fc portion of IgG (Fc gamma RII). The data presented in this study suggest that IgG charge constitutes a critical property that conditions the ability of IC to trigger platelet activation.

scholarly journals Effects of soluble immune complexes on Fc receptor- and C3b receptor-mediated phagocytosis by macrophages.

1980 ◽  
Vol 152 (4) ◽  
pp. 905-919 ◽  
Author(s):  
F M Griffin
Keyword(s):  
Immune Complexes ◽  
Fc Receptors ◽  
Fc Receptor ◽  
Complement Receptor ◽  
Complement Receptors ◽  
Phagocytic Function ◽  
Receptor Function ◽  
Coated Particles ◽  
C3b Receptor ◽  
Soluble Immune Complexes

The effects of ingestion of soluble immune complexes upon macrophage phagocytic function was studied. Ingestion of immune complexes severely impaired the macrophage's ability to ingest IgG-coated particles but did not alter its ability to interact with particles by means other than its Fc receptors. Treatment of macrophages that had ingested immune complexes with supernates containing the previously described lymphokine that augments macrophage complement receptor function failed to enhance the cells' interaction with either IgG-coated erythrocytes or zymosan particles but markedly enhanced their ability to phagocytize via their complement receptors. The possible significance of these findings in immunologically mediated inflammation is discussed.

Influence of C1q on the Interaction of Model Immune Complexes with Human Platelets

1995 ◽  
Vol 76 (2) ◽  
pp. 127-134 ◽  
Author(s):  
J.A. Sloand ◽  
R.L. Mehta ◽  
G. Schmer ◽  
S.I. Rosenfeld
Keyword(s):  
Immune Complexes ◽  
Human Platelets

Interaction of immune complexes with Fc receptors in mesangial cells: A potential target for the treatment of IgA nephropathy

Nephrology ◽  
1997 ◽  
Vol 3 (1) ◽  
pp. 95-101 ◽  
Author(s):  
C. GÓMEZ-GUERRERO ◽  
N. DUQUE ◽  
MJ LÓPEZ-ARMADA ◽  
MT CASADO ◽  
F. VIVANCO ◽  
...  
Keyword(s):  
Iga Nephropathy ◽  
Immune Complexes ◽  
Mesangial Cells ◽  
Fc Receptors ◽  
Potential Target

scholarly journals Platelet Activation in Heparin-Induced Thrombocytopenia is Followed by Platelet Death via Complex Apoptotic and Non-Apoptotic Pathways

2020 ◽  
Vol 21 (7) ◽  
pp. 2556
Author(s):  
Elmira R. Mordakhanova ◽  
Tatiana A. Nevzorova ◽  
Gulnaz E. Synbulatova ◽  
Lubica Rauova ◽  
John W. Weisel ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Immune Complexes ◽  
Gel Filtration ◽  
Human Platelets ◽  
Platelet Factor 4 ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Mitochondrial Membrane Depolarization ◽  
Low Platelet Count ◽  
Apoptotic Pathways

Heparin-induced thrombocytopenia (HIT) is an adverse drug reaction characterized by thrombocytopenia and a high risk for venous or arterial thrombosis. HIT is caused by antibodies that recognize complexes of platelet factor 4 and heparin. The pathogenic mechanisms of this condition are not fully understood. In this study, we used flow cytometry, fluorimetry, and Western blot analysis to study the direct effects of pathogenic immune complexes containing platelet factor 4 on human platelets isolated by gel-filtration. HIT-like pathogenic immune complexes initially caused pronounced activation of platelets detected by an increased expression of phosphatidylserine and P-selectin. This activation was mediated either directly through the FcγRIIA receptors or indirectly via protease-activated receptor 1 (PAR1) receptors due to thrombin generated on or near the surface of activated platelets. The immune activation was later followed by the biochemical signs of cell death, such as mitochondrial membrane depolarization, up-regulation of Bax, down-regulation of Bcl-XL, and moderate activation of procaspase 3 and increased calpain activity. The results show that platelet activation under the action of HIT-like immune complexes is accompanied by their death through complex apoptotic and calpain-dependent non-apoptotic pathways that may underlie the low platelet count in HIT.

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