The uptake by blood-borne phagocytes of monosodium urate is dependent on heat-labile serum factor(s) and divalent cations

Accumulation in tissues of post-apoptotic cells is a feature frequently observed in patients with systemic lupus erythematosus and in murine models of systemic autoimmune diseases. One of the endogenous danger molecules released by secondarily necrotic cells is monosodium urate (MSU), which is alrea...

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Bibliographic Details
Published in:Autoimmunity (Chur, Switzerland) Switzerland), 2010-05, Vol.43 (3), p.236-238
Main Authors: Schorn, Christine, Strysio, Moritz, Janko, Christina, Munoz, Luis E., Schett, Georg, Herrmann, Martin
Format: Article
Language:English
Subjects:
blood-borne phagocytes
Cations, Divalent - blood
Cations, Divalent - immunology
cytokines
Cytokines - immunology
Gout - blood
Gout - immunology
Humans
Inflammation
Lupus Erythematosus, Systemic - blood
Lupus Erythematosus, Systemic - immunology
MSU
Phagocytes - immunology
Phagocytes - metabolism
SLE
Uric Acid - blood
Uric Acid - immunology
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Summary:Accumulation in tissues of post-apoptotic cells is a feature frequently observed in patients with systemic lupus erythematosus and in murine models of systemic autoimmune diseases. One of the endogenous danger molecules released by secondarily necrotic cells is monosodium urate (MSU), which is already established to be the causative agent of gout. Here, we show that MSU is taken up by eosinophils, neutrophils and monocytes in a process involving (a) heat-labile serum factor(s) and divalent cations. The uptake induces the release of the pro-inflammatory cytokines IL-1β/IL-18/TNFα and IL-6/IL-8 by monocytes and PMN, respectively.
ISSN:0891-6934
1607-842X
DOI:10.3109/08916930903510948