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2 raisons identifiées
Praticien-chercheur
14 articles scientifiques publiés — formation continue solide
Délais de RDV courts dans la région
119.2 rhumatos / 100 000 hab. — département bien doté
✨ Génération du profil synthétique IA en cours…
CABINET DU DR CHRISTOPHE STEINBERG
57 BIS RUE DILLARD, 76680 ST SAENS
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Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).
Arthritis and rheumatism · 2008
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.
New York state journal of medicine · 1947
Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).
Arthritis and rheumatism · 2008 · Journal Article
Savarese E, Steinberg C, Pawar RD, Reindl W, et al.
New York state journal of medicine · 1975 · Journal Article
Steinberg CL
New York state journal of medicine · 1963 · Journal Article
STEINBERG CL
The American journal of the medical sciences · 1958 · Journal Article
STEINBERG CL, ROODENBURG AI
Annals of internal medicine · 1953 · Journal Article
STEINBERG CL
A.M.A. archives of surgery · 1951 · Journal Article
STEINBERG CL
Journal of the American Medical Association · 1951 · Journal Article
STEINBERG CL, ROODENBURG AI
Journal of insurance medicine · 1949 · Journal Article
STEINBERG CL
Journal of the American Medical Association · 1948 · Journal Article
STEINBERG CL
Annals of the rheumatic diseases · 1948 · Journal Article
STEINBERG CL
New York state journal of medicine · 1947 · Journal Article
STEINBERG CL
The Medical clinics of North America · 1946 · Journal Article
STEINBERG CL
Berliner und Munchener tierarztliche Wochenschrift · 2003 · English Abstract
Lahrmann KH, Steinberg C, Dahms S, Heller P
Annals of internal medicine · 1956 · Journal Article
STEINBERG CL, ROODENBURG AI