M. Docteur GERARD LECLERCQ

Thèses universitaires

• Osteodensitometrie a ultrasons : etude de la reproductibilite et correlation avec l'absorptiometrie a rayons x

  1992
  Médecine🎓 Amiens

  Direction : Jean-Luc Sebert

Source : catalogue national des thèses theses.fr (ABES). Ne couvre que les doctorats / HDR — les thèses d'exercice (DES) sont archivées dans les SCD universitaires.

Localisation

Adresses géocodées via la Base Adresse Nationale (api-adresse.data.gouv.fr). Précision indicative.

Lieu de consultation

• CABINET DU DR GERARD LECLERCQ

  13 BOULEVARD VICTOR HUGO, 62100 Calais

  ☎ 0321347783Libéral
  53 m

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Tarifs & secteur de conventionnement

Prendre rendez-vous & contact

Lien Doctolib = recherche Google site:doctolib.fr (le 1er résultat est presque toujours le profil correct s'il existe).

Top publications · les plus citées

• 1

  Activated CD4+CD25+ regulatory T cells inhibit osteoclastogenesis and collagen-induced arthritis

  Annals of the rheumatic diseases · 2009

  📚 132 citations🎯 RCR 3.05Top 16% NIH
• 2

  Defective CD4+CD25+ regulatory T cell functioning in collagen-induced arthritis: an important factor in pathogenesis, counter-regulated by endogenous IFN-gamma

  Arthritis research & therapy · 2005

  📚 131 citations🎯 RCR 2.55Top 20% NIH🔓 Open Access

  Lire l'abstract Crossref ↓

  AbstractMice with a deficiency in IFN-γ or IFN-γ receptor (IFN-γR) are more susceptible to collagen-induced arthritis (CIA), an experimental autoimmune disease that relies on the use of complete Freund's adjuvant (CFA). Here we report that the heightened susceptibility of IFN-γR knock-out (KO) mice is associated with a functional impairment of CD4+CD25+ Treg cells. Treatment of wild-type mice with depleting anti-CD25 antibody after CFA-assisted immunisation with collagen type II (CII) significantly accelerated the onset of arthritis and increased the severity of CIA. This is an indication of a role of Treg cells in the effector phase of CIA. IFN-γR deficiency did not affect the number of CD4+CD25+ T cells in the central and peripheral lymphoid tissues. In addition, CD4+CD25+ T cells isolated from naive IFN-γR KO mice had a normal potential to suppress T cell proliferation in vitro. However, after immunisation with CII in CFA, the suppressive activity of CD4+CD25+ T cells became significantly more impaired in IFN-γR-deficient mice. Moreover, expression of the mRNA for Foxp3, a highly specific marker for Treg cells, was lower. We further demonstrated that the effect of endogenous IFN-γ, which accounts for more suppressive activity in wild-type mice, concerns both Treg cells and accessory cells. Our results demonstrate that the decrease in Treg cell activity in CIA is counter-regulated by endogenous IFN-γ.

• 3

  Systemic juvenile idiopathic arthritis-like syndrome in mice following stimulation of the immune system with Freund's complete adjuvant: regulation by interferon-γ

  Arthritis & rheumatology (Hoboken, N.J.) · 2014

  📚 77 citations🎯 RCR 2.26Top 23% NIH

  Lire l'abstract Crossref ↓

  ObjectiveSystemic juvenile idiopathic arthritis (JIA) is unique among the rheumatic diseases of childhood, given its distinctive systemic inflammatory character. Inappropriate control of innate immune responses following an initially harmless trigger is thought to account for the excessive inflammatory reaction. The aim of this study was to generate a similar systemic inflammatory syndrome in mice by injecting a relatively innocuous, yet persistent, immune system trigger: Freund's complete adjuvant (CFA), containing heat‐killed mycobacteria.MethodsGiven the central role of interferon‐γ (IFNγ) in immune regulation, we challenged wild‐type (WT) and IFNγ‐knockout (KO) BALB/c mice with CFA, and analyzed their clinical symptoms and biologic characteristics. The production of cytokines and the effects of anticytokine antibodies were investigated.ResultsIn WT mice, CFA injection resulted in splenomegaly, lymphadenopathy, neutrophilia, thrombocytosis, and increased cytokine expression. In the absence of IFNγ, these symptoms were more pronounced and were accompanied by weight loss, arthritis, anemia, hemophagocytosis, abundance of immature blood cells, and increased levels of interleukin‐6 (IL‐6), all of which are reminiscent of the symptoms of systemic JIA. CFA‐challenged IFNγ‐KO mice showed increased expression of IL‐17 by CD4+ T cells and by innate γ/δ T cells. Inflammatory and hematologic changes were prevented by treatment with anti–IL‐12/IL‐23p40 and anti–IL‐17 antibodies.ConclusionImmune stimulation of IFNγ‐KO mice with CFA produces a systemic inflammatory syndrome reflecting the clinical, biologic, and histopathologic picture of systemic JIA. The protective function of IFNγ in preventing anemia and overall systemic inflammation is a striking observation. The finding that both adaptive and innate T cells are important sources of IL‐17 may be of relevance in the pathogenesis of systemic JIA.

Publications scientifiques (11) — classées par pathologie

Source PubMed · Recherche par auteur (homonymes possibles, vérifier l'affiliation).

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