Studies on the mode of reaction of the first component of complement with platelets: Interaction between the collagen-like portion of C1q and platelets

Jl, Wautier; Souchon, H.; Reid, Kenneth B.M.; Peltier, A; Caen, J

doi:10.1016/0019-2791(77)90351-2

Cited by 41 publications

(7 citation statements)

References 9 publications

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“…The experiments using collagen-like stalks or globular heads of Clq demonstrate that ClqR binds to the collagen-like stalk of Clq. These observations are compatible with the findings of others [ll, 16,[35][36][37] and with our own results [12]. Macromolecular C l is composed of Clq, Clr and Cls, held together by cations [38].…”

Section: Discussionsupporting

confidence: 95%

Regulation of the function of the first component of complement by human C1q receptor

Berg

Faber-Krol

et al. 1995

Eur J Immunol

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A membrane-associated receptor for the C1q subcomponent of complement is widely distributed among different cell types. While a number of possible physiological functions of the C1q receptor (C1qR) on different cell types have been described, the way in which C1qR regulates complement activity remains unclear. This report describes the mechanism by which C1qR regulates activation of the first component of complement, C1. Using purified components of complement, we were able to show that membrane-associated C1qR as well as detergent-solubilized C1qR, purified from polymorphonuclear leukocytes, human umbilical vein endothelial cells or an endothelial cell line, EA.hy 926, are able to inhibit complement-mediated lysis of C1q-sensitized erythrocytes. Using hemolytic assays, we were able to demonstrate that C1qR prevents the association of C1q with C1r and C1s to form macromolecular C1. In addition, incubation of C1qR with the collagen-like stalks, but not with the globular heads of C1q, inhibits the effect of C1qR. This demonstrates that C1qR exerts its complement inhibitory effect by binding to the collagen-like stalk of C1q. No complement regulatory effect of C1qR was observed on preformed macromolecular C1. These data suggest that besides such-well-known complement regulatory molecules as CD55 (DAF), CD46 (MCP), CD35 (CR1) and CD59 (HRF), C1qR too is able to regulate complement activity.

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Section: Discussionsupporting

confidence: 95%

Regulation of the function of the first component of complement by human C1q receptor

Berg

Faber-Krol

et al. 1995

Eur J Immunol

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“…In addition, CR4, also a receptor for iC3b, is expressed on platelets but so far with unclear function (Vik and Fearon, 1987 ). Besides the aforementioned C3-fragment receptors, platelet expressed C1q receptors gC1qR/p33 and cC1qR were shown to mediate platelet aggregating and activating effects (Wautier et al, 1977 ; Peerschke and Ghebrehiwet, 1997 , 2001 ). Also receptors for anaphylatoxins C3a and C5a, which are generated further downstream in the complement activation cascade, are found on platelets.…”

Section: Platelets and The Complement Systemmentioning

confidence: 99%

Platelets and the complement cascade in atherosclerosis

2015

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Atherosclerosis and its late sequels are still the number one cause of death in western societies. Platelets are a driving force not only during the genesis of atherosclerosis, but especially in its late stages, as evidenced by complications such as arterial thrombosis, myocardial infarction, and ischemic stroke. Atherosclerosis is increasingly recognized as an inflammatory disease, influenced by various immune mechanisms. The complement system is part of our innate immune system, and its diverse roles in atherosclerosis have become evident over the past years. In this review we identify points of intersection between platelets and the complement system and discuss their relevance for atherosclerosis. Specifically, we will focus on roles for platelets in the onset as well as progression of the disease, a possible dual role for complement in the genesis and development of atherosclerosis, and review emerging literature revealing previously unrecognized cross-talk between platelets and the complement system and discuss its possible impact for atherosclerosis. Finally, we identify limitations of current research approaches and discuss perspectives of complement modulation in the control of the disease.

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“…Expression of iC3b receptor CR4 has also been reported (53), but its physiological role remains unclear. Not only C3-fragment receptors have been described on platelets, also C1q-receptor expression has been documented, specifically gC1qR/p33 and cC1qR with affinity for the C1q globular heads and its collagenous tail, respectively, mediating platelet aggregating and activating effects (54)(55)(56). There are also strong indications that anaphylatoxin C3a and C5a receptors are present on human platelets, and C3a and its derivative C3adesArg induce platelet activation and aggregation in vitro, whereas in vivo data are not available to date (57,58) Interaction between platelets and complement may also occur via receptors not typically regarded as CR, such as P-selectin (57).…”

Section: Modes Of Interactions Between the Complement System And Platmentioning

confidence: 99%

Crosstalk between platelets and the complement system in immune protection and disease

Verschoor¹,

Langer²

2013

Thromb Haemost

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Platelets have a central function in repairing vascular damage and stopping acute blood loss. They are equally central to thrombus formation in cardiovascular diseases such as myocardial infarction and ischaemic stroke. Beyond these classical prothrombotic diseases, immune mediated pathologies such as haemolytic uraemic syndrome (HUS) or paroxysmal nocturnal haemoglobinuria (PNH) also feature an increased tendency to form thrombi in various tissues. It has become increasingly clear that the complement system, part of the innate immune system, has an important role in the pathophysiology of these diseases. Not only does complement influence prothrombotic disease, it is equally involved in idiopathic thrombocytopenic purpura (ITP), an autoimmune disease characterised by thrombocytopenia. Thus, there are complex interrelationships between the haemostatic and immune systems, and platelets and complement in particular. Not only does complement influence platelet diseases such as ITP, HUS and PNH, it also mediates interaction between microbes and platelets during systemic infection, influencing the course of infection and development of protective immunity. This review aims to provide an integrative overview of the mechanisms underlying the interactions between complement and platelets in health and disease.

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Studies on the mode of reaction of the first component of complement with platelets: Interaction between the collagen-like portion of C1q and platelets

Cited by 41 publications

References 9 publications

Regulation of the function of the first component of complement by human C1q receptor

Regulation of the function of the first component of complement by human C1q receptor

Platelets and the complement cascade in atherosclerosis

Crosstalk between platelets and the complement system in immune protection and disease

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