Selective induction of pentraxin 3, a soluble innate immune pattern recognition receptor, in infectious episodes in patients with haematological malignancy

Pentraxins are a superfamily of conserved proteins induced in response to microbial and inflammatory stimuli. Members of this family include C-reactive protein (CRP) and serum amyloid P component, collectively known as the classical short pentraxins, and the more recently discovered pentraxin 3 (PTX...

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Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 112(2004), 3 vom: 12. Sept., Seite 221-4
1. Verfasser: al-Ramadi, Basel K (VerfasserIn)
Weitere Verfasser: Ellis, Michael, Pasqualini, Fabio, Mantovani, Alberto
Format: Aufsatz
Sprache:English
Veröffentlicht: 2004
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Serum Amyloid P-Component PTX3 protein 148591-49-5 C-Reactive Protein 9007-41-4
Beschreibung
Zusammenfassung:Pentraxins are a superfamily of conserved proteins induced in response to microbial and inflammatory stimuli. Members of this family include C-reactive protein (CRP) and serum amyloid P component, collectively known as the classical short pentraxins, and the more recently discovered pentraxin 3 (PTX3), a member of the closely related subfamily of the long pentraxins. PTX3 has been shown to be produced in response to microbial infections, and highly elevated levels were reported in patients with sepsis. In this study, PTX3 levels were evaluated in sera of a group of patients with haematological malignancy. Our findings indicate that serum PTX3 was elevated in only 1/11 afebrile episodes, despite evidence of mucositis (median 1.39), in 10/10 episodes of blood stream or target organ infections (median 7.2) but, surprisingly, was normal in 5/5 episodes of invasive aspergillosis (median 1.39). The data suggest that serum PTX3 levels are elevated selectively in response to infection. These disparate responses require further study
Beschreibung:Date Completed 22.09.2004
Date Revised 10.12.2019
published: Print
Citation Status MEDLINE
ISSN:1521-6616