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NDT Advance Access originally published online on September 5, 2006
Nephrology Dialysis Transplantation 2006 21(11):3062-3073; doi:10.1093/ndt/gfl336
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Expression and regulation of Toll-like receptors in lupus-like immune complex glomerulonephritis of MRL-Fas(lpr) mice

Prashant S. Patole*, Rahul D. Pawar*, Maciej Lech, Daniel Zecher, Holger Schmidt, Stephan Segerer, Andreas Ellwart, Anna Henger, Matthias Kretzler and Hans-Joachim Anders

Nephrological Center, Medical Policlinic, University of Munich, Munich, Germany

Correspondence and offprint requests to: Hans-Joachim Anders, MD, Medizinische Poliklinik, Universität München, Pettenkoferstr. 8a 80336 München, Germany. Email: hjanders{at}med.uni-muenchen.de

Background. How microbial infections exacerbate immune complex glomerulonephritis remains speculative. Toll-like receptors (TLRs) may be involved in this phenomenon, because TLRs have potent immunostimulatory functions when exposed to selected pathogen-associated molecules.

Methods. We addressed this issue by characterizing the expression of TLR1–9 in MRLlpr/lpr mice that spontaneously develop immune complex glomerulonephritis as part of a systemic lupus-like autoimmune syndrome.

Results. Five-week-old healthy MRLlpr/lpr mice expressed TLR3 mRNA in kidneys at comparable levels as in the spleen, while all other TLRs were expressed at low levels in the kidney. In 20-week-old nephritic MRLlpr/lpr mice, renal mRNA levels had increased for TLR1–9. Renal TLR mRNA originated at least in part from glomeruli as evidenced by real-time RT-PCR from laser capture microdissected glomeruli. Immunostaining for TLR3, TLR7 and TLR9 revealed their expression by F4/80-positive infiltrating macrophages in 20-week-old nephritic MRLlpr/lpr mice. In addition, TLR3 localized to glomerular mesangial cells. Cultured mesangial cells expressed TLR1–4 and TLR6, while murine macrophages expressed TLR1–9. TNF-{alpha} and IFN-{gamma} induced TLR2, TLR3 and TLR6 mRNA in mesangial cells, while they down-regulated TLR1–9 mRNA in macrophages. Stimulation of both cell types with ligands for TLR1–4, TLR5, TLR7 and TLR9 induced IL-6 production consistent with their respective TLR expression patterns. TNF-{alpha} and IFN-{gamma} enhanced ligand-induced IL-6 production in both cell types irrespective of their modulatory effect on respective TLR mRNA levels.

Conclusion. Thus, cell-type-specific expression and regulation of TLRs may be involved in infection-associated exacerbation of immune complex glomerulonephritis of MRLlpr/lpr mice.

Keywords: autoimmune diseases; innate immunity; kidney; lupus; Toll-like receptor

* The authors wish it to be known that, in their opinion, the first two authors contributed equally to this work.


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