Directing autoimmunity to nucleoprotein particles: the impact of dendritic cells and interferon alpha in lupus - PubMed (original) (raw)
Comment
Directing autoimmunity to nucleoprotein particles: the impact of dendritic cells and interferon alpha in lupus
John A Hardin. J Exp Med. 2003.
No abstract available
Figures
Figure 1.
Hypothetical model for the role of IFN-α in propagating autoimmunity to chromatin. An exogenous event such as a viral infection triggers IFN-α secretion, thus simultaneously augmenting apoptosis, monocyte maturation, and T cell priming. In an individual with a permissive genetic make-up, T cell responses to chromatin components such as histones are induced providing the necessary help for specific B cell responses to components such as DNA. Once initiated, the response is perpetuated endogenously by the ability of immune complexes based on anti-DNA antibodies (and possibly other specificities) to stimulate secretion of IFN-α by plasmacytoid DCs. Cell injury secondary to these complexes results in apoptotic cell debris that contributes to enhanced loading of nucleoproteins into DCs. Accelerated granulopoiesis may contribute to the burden of this material and represent an important source of nucleoprotein autoantigens as these cells turn over.
Comment on
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