📇 Rhumatologue · ST SAENS · (76) · Hospitalier

M CHRISTOPHE STEINBERG

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14 articles scientifiques publiés — formation continue solide
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119.2 rhumatos / 100 000 hab. — département bien doté

Rhumatologue

📍 ST SAENS (76)HospitalierRPPS 10001915247

✨ Génération du profil synthétique IA en cours…

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CABINET DU DR CHRISTOPHE STEINBERG
57 BIS RUE DILLARD, 76680 ST SAENS
☎ 0235322392Activité de soin et de pharmacie

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Requirement of Toll-like receptor 7 for pristane-induced production of autoantibodies and development of murine lupus nephritis

Arthritis and rheumatism · 2008

📚 111 citations🎯 RCR 2.25Top 23% NIH

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AbstractObjectiveThe detection of high titers of antibodies against small nuclear ribonucleoproteins (snRNP) is a diagnostic finding in patients in whom systemic lupus erythematosus (SLE) is suspected. Endogenous RNA molecules within snRNP trigger Toll‐like receptor 7 (TLR‐7) activation in B cells and dendritic cells, leading to anti‐snRNP antibody production, which is associated with the development of immune complex nephritis in SLE. The purpose of this study was to investigate the role of TLR‐7 in anti‐snRNP antibody production and renal disease in SLE induced by an exogenous factor in the absence of genetic predisposition, using the pristane‐induced murine lupus model.MethodsSerum autoantibodies, IgG isotypes, and cytokine levels in pristane‐treated wild‐type and TLR‐7–deficient mice were analyzed by enzyme‐linked immunosorbent assay. Histopathologic changes in mouse kidneys were determined by light immunofluorescence microscopy. Cell subsets in splenocytes and peritoneal lavage cells from the mice were examined by flow cytometry.ResultsWe found that anti‐snRNP antibody production induced by pristane treatment was entirely dependent on the expression of TLR‐7, whereas anti–double‐stranded DNA antibody production was not affected by a lack of TLR‐7. Impaired anti‐snRNP antibody production in TLR‐7–deficient mice was paralleled by lower levels of glomerular IgG and complement deposits, as well as less severe glomerulonephritis.ConclusionTLR‐7 is specifically required for the production of RNA‐reactive autoantibodies and the development of glomerulonephritis in pristane‐induced murine lupus, a model of environmentally triggered SLE in the absence of genetic susceptibility to autoimmunity. Specific interference with TLR‐7 activation by endogenous TLR‐7 ligands may therefore be a promising novel strategy for the treatment of SLE.

Fibrositis (muscular rheumatism) including Dupuytren's contracture: a new method of treatment

New York state journal of medicine · 1947

📚 27 citations

Splenectomy in rheumatoid arthritis

Annals of internal medicine · 1953

📚 17 citations

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M CHRISTOPHE STEINBERG

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Publications scientifiques (14) — classées par pathologie

Transversal12

Épidémiologie & registres1

Lupus1

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