A new function for platelets: IgE-dependent killing of schistosomes

Joseph, M.; Auriault, C.; Càpron, André; Vorng, Han; Viens, P.

doi:10.1038/303810a0

Cited by 286 publications

(143 citation statements)

References 5 publications

Supporting

Mentioning

136

Contrasting

Unclassified

Order By: Relevance

“…Furthermore, immunization of rats according to protocols leading to IgE production (16,17), passive transfer of IgE rich-serum from S. mansoni-infected rats or of anti-S. mansoni rat IgE mAb to naive recipient rats (18) led to a significant level of protection to a challenge infection. Such a protective effect was also observed when platelets (19), eosinophils, or macrophages (20), obtained from infected animals and bearing cytophilic IgE, were transferred to naive rats. In mice, various studies about the protective role of IgE in schistosomiasis have led to divergent conclusions (21)(22)(23)(24)(25).…”

mentioning

confidence: 80%

Expression of a Functional FcεRI on Rat Eosinophils and Macrophages

Dombrowicz

Quatannens

Papin

et al. 2000

The Journal of Immunology

Self Cite

View full text Add to dashboard Cite

Besides its crucial role in type I hypersensitivity reactions, IgE is involved in anti-parasite immunity. This role has been clearly demonstrated in both human and rat schistosomiasis, but remains controversial in the mouse. Since the cellular distribution of the high affinity IgE receptor, FcεRI, differs in humans and mice, it might explain the differences in effector function of IgE between the two species. In humans, eosinophils and macrophages induce IgE-dependent cytotoxicity toward Schistosoma mansoni larvae, which involves FcεRI in the case of eosinophils. In the present study, we have investigated the expression and function of FcεRI in rat eosinophils and macrophages. We demonstrate, by flow cytometry, fluorescence microscopy, and Western blot analysis, that in rats, as in humans, a functional αγ2 trimeric FcεRI is expressed on eosinophils and macrophages. We also show that these two cell types can induce IgE-mediated, FcεRI-dependent cellular cytotoxicity toward schistosomula. These results thus provide a molecular basis for the differences observed between rat and mouse regarding IgE-mediated anti-parasite immunity.

show abstract

mentioning

confidence: 80%

Expression of a Functional FcεRI on Rat Eosinophils and Macrophages

Dombrowicz

Quatannens

Papin

et al. 2000

The Journal of Immunology

Self Cite

View full text Add to dashboard Cite

show abstract

“…However, it is apparent that only a few platelets express both FceRI and FceRII simultaneously (Joseph et al, 1997), and these may represent a subset of platelets that react in a dichotic manner to inflammatory stimuli compared to 'normal' platelets. The involvement of platelets in allergic inflammation may well represent inappropriate actions of platelets commonly displayed in IgE-mediated immunity against helminth and protozoan parasitic infections (Joseph et al, 1983(Joseph et al, , 1985Momi et al, 2000). Platelet activation via FceRI has been shown to induce the release of 5-HT, ROS and RANTES, demonstrating that platelets may play an important role in the progression of allergic inflammation via IgE-dependent mechanisms (Joseph et al, 1986;Klouche et al, 1997).…”

Section: Platelet Involvement In Antigen Recognitionmentioning

confidence: 99%

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Pitchford

2007

British J Pharmacology

View full text Add to dashboard Cite

An alteration in the character and function of platelets is manifested in patients with inflammatory diseases, and these alterations have been dissociated from the well‐characterized involvement of platelets in thrombosis and haemostasis. Recent evidence reveals platelet activation is sometimes critical in the development of inflammation. The mechanisms by which platelets participate in inflammation are diverse, and offer numerous opportunities for future drug intervention. There is now acceptance that platelets act as innate inflammatory cells in immune responses, with roles as sentinel cells undergoing surveillance, responding to microbial invasion, orchestrating leukocyte recruitment, and migrating through tissue, causing damage and influencing repair processes in chronic disease. Some of these processes are targeted by drugs that are being developed to target platelet participation in atherosclerosis. The actions of platelets therefore influence the pathogenesis of diverse inflammatory diseases in various body compartments, encompassing parasitic and bacterial infection, allergic inflammation (especially asthma and rhinitis), and non‐atopic inflammatory conditions, for example, chronic obstructive pulmonary disease (COPD), rheumatoid arthritis (RA), inflammatory bowel disease (IBD) and atherosclerosis. This review will first discuss the evidence for platelet activation in these various inflammatory diseases, and secondly discuss the mechanisms by which this pathogenesis occurs and the various anti‐platelet agents which have been developed to combat platelet activation in atherosclerosis and their potential future use for the treatment of other inflammatory diseases.British Journal of Pharmacology (2007) 152, 987–1002; doi:10.1038/sj.bjp.0707364; published online 2 July 2007

show abstract

“…Platelets play a key role in blood clotting and the ATP hydrolysis product ADP is a major agonist of platelet recruitment and aggregation [14]. Additionally, platelets have been shown to be directly damaging to schistosomes [15]. The surface-exposed, nucleotide metabolizing ectoenzymes that are predicted to degrade extraneous ATP, could likewise act on ADP to prevent the host from mobilizing the blood coagulation machinery to activate platelets in their vicinity [9].…”

Section: Discussionmentioning

confidence: 99%

“…Medium containing ATP and lacking parasites was incubated as above and served as a control. To look for the release of ATPase activity from cultured parasites, groups of adults (12)(13)(14)(15) were first incubated in medium for 55 h at 5 % CO 2 and 37°C. Next, the parasites were removed and ATP (to 10 mM) was added to the medium.…”

Section: Smatpdase Assay: Atp Quantificationmentioning

confidence: 99%

“…In addition, ATP hydrolysis commonly leads to the generation of ADP and ADP is a major agonist of platelet recruitment and aggregation [14]. Furthermore, platelets themselves can damage schistosomes [15]. Therefore, the catabolism of exogenous ADP, in addition to ATP, would lead to the inhibition of platelet aggregation and thrombus formation around the worms.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Schistosome apyrase SmATPDase1, but not SmATPDase2, hydrolyses exogenous ATP and ADP

Da’dara¹,

Bhardwaj²,

Skelly³

2014

Purinergic Signalling

View full text Add to dashboard Cite

Schistosomes are parasitic worms that can live in the bloodstream of their vertebrate hosts for many years. It has been proposed that the worms impinge on host purinergic signalling by degrading proinflammatory molecules like ATP as well as prothrombotic mediators like ADP. This capability may help explain the apparent refractoriness of the worms to both immune elimination and thrombus formation. Three distinct ectoenzymes, expressed at the host-exposed surface of the worm's tegument, are proposed to be involved in the catabolism of ATP and ADP. These are alkaline phosphatase (SmAP), phosphodiesterase (SmNPP-5), and ATP diphosphohydrolase (SmATPDase1). It has recently been shown that only one of these enzymes-SmATPDase1-actually degrades exogenous ATP and ADP. However, a second ATP diphosphohydrolase homolog (SmATPDase2) is located in the tegument and has been reported to be released by the worms. It is possible that this enzyme too participates in the cleavage of exogenous nucleotide tri-and di-phosphates. To test this hypothesis, we employed RNA interference (RNAi) to suppress the expression of the schistosome SmATPDase1 and SmATPDase2 genes. We find that only SmATPDase1-suppressed parasites are significantly impaired in their ability to degrade exogenously added ATP or ADP. Suppression of SmATPDase2 does not appreciably affect the worms' ability to catabolize ATP or ADP. Furthermore, we detect no evidence for the secretion or release of an ATP-hydrolyzing activity by cultured parasites. The results confirm the role of tegumental SmATPDase1, but not SmADTPDase2, in the degradation of the exogenous proinflammatory and prothrombotic nucleotides ATP and ADP by live intravascular stages of the parasite.

show abstract

A new function for platelets: IgE-dependent killing of schistosomes

Cited by 286 publications

References 5 publications

Expression of a Functional FcεRI on Rat Eosinophils and Macrophages

Expression of a Functional FcεRI on Rat Eosinophils and Macrophages

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

Schistosome apyrase SmATPDase1, but not SmATPDase2, hydrolyses exogenous ATP and ADP

Contact Info

Product

Resources

About