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Authors: Gladigau, Gerd
Haselmayer, Philipp
Scharrer, Inge
Munder, Markus
Prinz, Nadine
Lackner, Karl J.
Schild, Hansjörg
Stein, Pamela
Radsak, Markus
Title: A role for Toll-like receptor mediated signals in neutrophils in the pathogenesis of the anti-phospholipid syndrome
Online publication date: 20-Oct-2022
Year of first publication: 2012
Language: english
Abstract: The anti-phospholipid syndrome (APS) is characterized by recurrent thrombosis and occurrence of anti-phospholipid antibodies (aPL). aPL are necessary, but not sufficient for the clinical manifestations of APS. Growing evidence suggests a role of innate immune cells, in particular polymorphonuclear neutrophils (PMN) and Toll-like receptors (TLR) to be additionally involved. aPL activate endothelial cells and monocytes through a TLR4-dependent signalling pathway. Whether this is also relevant for PMN in a similar way is currently not known. To address this issue, we used purified PMN from healthy donors and stimulated them in the presence or absence of human monoclonal aPL and the TLR4 agonist LPS monitoring neutrophil effector functions, namely the oxidative burst, phagocytosis, L-Selectin shedding and IL-8 production. aPL alone were only able to induce minor activation of PMN effector functions at high concentrations. However, in the additional presence of LPS the activation threshold was markedly lower indicating a synergistic activation pathway of aPL and TLR in PMN. In summary, our results indicate that PMN effector functions are directly activated by aPL and boosted by the additional presence of microbial products. This highlights a role for PMN as important innate immune effector cells that contribute to the pathophysiology of APS.
DDC: 610 Medizin
610 Medical sciences
Institution: Johannes Gutenberg-Universität Mainz
Department: FB 04 Medizin
Place: Mainz
Version: Published version
Publication type: Zeitschriftenaufsatz
License: CC BY
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Journal: PLoS one
Pages or article number: 1
Publisher: PLoS
Publisher place: Lawrence, Kan.
Issue date: 2012
ISSN: 1932-6203
Publisher URL:
Publisher DOI: 10.1371/journal.pone.0042176
Appears in collections:DFG-OA-Publizieren (2012 - 2017)

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