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Autoimmunity Volume 42, 2009 - Issue 4
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Mini Review

Apo material as a trigger for inflammation in systemic lupus erythematosus

Hanna Marie Meesmann Department of Medicine V, University of Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany
,
Marijo Parcina Department of Medical Microbiology and Hygiene, University of Heidelberg, Im Neuenheimer Feld 324, 69120, Heidelberg, Germany
,
Hanns-Martin Lorenz Department of Medicine V, University of Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany
,
Norbert Blank Department of Medicine V, University of Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, Germany
&
Martin Schiller Department of Medicine V, University of Heidelberg, Im Neuenheimer Feld 410, 69120, Heidelberg, GermanyCorrespondence[email protected]
Pages 251-253 | Received 18 Nov 2008, Accepted 07 Jan 2009, Published online: 13 Aug 2009
 
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Abstract

While several characteristics of systemic lupus erythematosus (SLE) have been investigated, the distinct pathogenetic mechanisms leading to autoimmunity and chronic inflammation are not understood yet. A central role for apo has been implicated in the pathogenesis of SLE and an increased rate of apo or a defective clearance of apo cells have repeatedly been described in SLE patients, which show elevated levels of alpha-interferon (αIFN) as well as an enhanced expression of αIFN-alpha inducible genes referred to as αIFN signature. Recent publications link αIFN and apo: apo cell-derived microparticles can directly stimulate plasmacytoid dendritic cells to secret αIFN. This review highlights the role of apo material as source for AAg and as a trigger for chronic inflammation in the pathogenesis of SLE.

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