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]

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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Apo material as a trigger for inflammation in systemic lupus erythematosus

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Apo material as a trigger for inflammation in systemic lupus erythematosus

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