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Showing 1–7 of 7 results
Advanced filters: Author: Julien Zuber Clear advanced filters

  • Postrenal transplant hemolytic uremic syndrome (HUS) can occur as a recurrent orde novodisease. Improved understanding of the mechanisms by which atypical HUS occurs after transplantation should result in the improved management of affected patients. In this Review, Zuber and colleagues discuss recent advances in our understanding of the pathogenesis of atypical HUS and describe diagnostic and therapeutic considerations with regard to renal transplantation in these patients.

    • Julien Zuber
    • Moglie Le Quintrec
    • Christophe Legendre
    Reviews
    Nature Reviews Nephrology
    Volume: 7, P: 23-35

  • Zuber and colleagues from Paris describe a case of diabetes that developed after renal transplantation in a young, white, nonobese man. Genetic screening detected a newly described deletion in the gene encoding hepatocyte nuclear factor 1 homeobox B,HNF1B, indicating that mutations in HNF1Bmight account for some 'unexpected' cases of new-onset diabetes after transplantation. Minimization of tacrolimus exposure and withdrawal of steroids markedly reduced the patient's insulin requirement.

    • Julien Zuber
    • Christine Bellanné-Chantelot
    • Danièle Dubois-Laforgue
    Reviews
    Nature Reviews Nephrology
    Volume: 5, P: 480-484

  • Here, Zuber et al., on behalf of the French Study Group for aHUS/C3G, discuss the role of eculizumab in the treatment of atypical haemolytic uraemic syndrome (aHUS). They review data from case reports and preliminary data from prospective trials, present their opinions, and describe issues that require further study. In addition, they discuss the potential use of eculizumab in C3 glomerulopathies.

    • Julien Zuber
    • Fadi Fakhouri
    • Véronique Frémeaux-Bacchi
    Reviews
    Nature Reviews Nephrology
    Volume: 8, P: 643-657

  • Chimeric antigen receptor engineering in T cells has been shown to be of great potential therapeutic benefit in a range of immune pathologies, although the functionality of such cell therapies can be limited due to tonic signalling and the induction of dysfunction. Here the authors show transient inhibition of mTOR can rescue their 41-BB-CAR-Tregs from tonic signalling-induced dysfunction.

    • Baptiste Lamarthée
    • Armance Marchal
    • Julien Zuber
    ResearchOpen Access
    Nature Communications
    Volume: 12, P: 1-19

  • FOXP3 deficiency leads to dramatic loss of immune homeostasis. This multicenter collaborative group finds that loss of FOXP3 function only disrupts a few core genes, but this unmasks a degree of systemic inflammation, and it is this environment that then strongly perturbs Treg cells.

    • David Zemmour
    • Louis-Marie Charbonnier
    • Christophe Benoist
    Research
    Nature Immunology
    Volume: 22, P: 607-619