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Glomerular expression of toll-like receptor-9 in lupus nephritis but not in normal kidneys: implications for the amplification of the inflammatory response

Laboratory of Autoimmunity and Inflammation, Rheumatology, Clinical Immunology and Allergy, Medical School, University of Crete, Greece

M Tzardi

Department of Pathology, Medical School, University of Crete, Greece

G Bertsias

Laboratory of Autoimmunity and Inflammation, Rheumatology, Clinical Immunology and Allergy, Medical School, University of Crete, Greece

E Sotsiou

Department of Pathology, Evangelismos Hospital, Athens, Greece

DT Boumpas

Laboratory of Autoimmunity and Inflammation, Rheumatology, Clinical Immunology and Allergy, Medical School, University of Crete, Greeceboumpasd{at}med.uoc.gr

Toll-like receptors recognising self-derived nucleic acids may participate in the pathogenesis of autoimmune diseases. Following the description of an enhanced population of toll-like receptor-9 (TLR-9) expressing auto-antibody producing B lymphocytes in active lupus, we explored the expression of TLR-9 in the renal tissue of patients with lupus. TLR-9 expression was studied in the kidneys of 12 lupus and 10 control samples from macroscopically unaffected areas of patients with renal adenocarcinoma by immunohistochemistry. A semiquantitative score was assigned separately for tubular, interstitial and glomerular expression. TLR-9 was expressed in the renal tubules and interstitial tissue in both patients with lupus and controls. Six of 12 patients with lupus with proliferative or membranous nephritis – as compared to none of the controls – exhibited both tubulointerstitial and glomerular TLR-9 expression. Biopsies with glomerular TLR-9 expression had a higher activity index (mean ± SD, 6.3 ± 3.5 in the presence of TLR-9 glomerular expression as compared to 1.3 ± 1.8 in its absence, P = 0.015, t-test). This study documents for the first time the up-regulation of TLR-9 within the glomerulus of patients with lupus nephritis. Activation of TLR-9 expressing glomerular cells by endogenous nucleic acids (nucleosomes) may amplify the inflammatory response.

Key Words: nephritis • renal lupus • TLRs

Lupus, Vol. 18, No. 9, 831-835 (2009)
DOI: 10.1177/0961203309103054


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