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  1. Article ; Online: Tolérance en transplantation par chimérisme mixte.

    Zuber, Julien

    Nephrologie & therapeutique

    2017  Volume 13 Suppl 1, Page(s) S127–S130

    Abstract: Three pilot studies have offered proof-of-concept that operational tolerance can be induced through mixed chimerism in recipients of combined kidney and hematopoietic cell transplants from the same donor. In two studies, sustained mixed chimerism was ... ...

    Title translation Transplant tolerance through mixed chimerism.
    Abstract Three pilot studies have offered proof-of-concept that operational tolerance can be induced through mixed chimerism in recipients of combined kidney and hematopoietic cell transplants from the same donor. In two studies, sustained mixed chimerism was induced allowing safe and rejection-free immunosuppression withdrawal. However, this success came at heavy toll, requiring harsh cytoreductive regimen and a balance tipped toward graft-versus-host reactivity. Hence, achievement of durable chimerism in humans is not devoid of a significant risk of graft-versus-host disease. In contrast, transient mixed chimerism can be induced with non-myeloablative and a less cytotoxic regimen, leading to transplant tolerance, whose underpinning mechanisms are more complex, involving T cell exhaustion, peripheral deletion and suppression.
    Language French
    Publishing date 2017-04
    Publishing country France
    Document type English Abstract ; Journal Article
    ZDB-ID 2229575-6
    ISSN 1872-9177 ; 1769-7255
    ISSN (online) 1872-9177
    ISSN 1769-7255
    DOI 10.1016/j.nephro.2017.01.017
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    Zs.A 6298: Show issues Location:
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  2. Article ; Online: Targeting the Complement Pathway in Kidney Transplantation.

    Golshayan, Dela / Schwotzer, Nora / Fakhouri, Fadi / Zuber, Julien

    Journal of the American Society of Nephrology : JASN

    2023  Volume 34, Issue 11, Page(s) 1776–1792

    Abstract: The complement system is paramount in the clearance of pathogens and cell debris, yet is increasingly recognized as a key component in several pathways leading to allograft injury. There is thus a growing interest in new biomarkers to assess complement ... ...

    Abstract The complement system is paramount in the clearance of pathogens and cell debris, yet is increasingly recognized as a key component in several pathways leading to allograft injury. There is thus a growing interest in new biomarkers to assess complement activation and guide tailored therapies after kidney transplantation (KTx). C5 blockade has revolutionized post-transplant management of atypical hemolytic uremic syndrome, a paradigm of complement-driven disease. Similarly, new drugs targeting the complement amplification loop hold much promise in the treatment and prevention of recurrence of C3 glomerulopathy. Although unduly activation of the complement pathway has been described after brain death and ischemia reperfusion, any clinical attempts to mitigate the ensuing renal insults have so far provided mixed results. However, the intervention timing, strategy, and type of complement blocker need to be optimized in these settings. Furthermore, the fast-moving field of ex vivo organ perfusion technology opens new avenues to deliver complement-targeted drugs to kidney allografts with limited iatrogenic risks. Complement plays also a key role in the pathogenesis of donor-specific ABO- and HLA-targeted alloantibodies. However, C5 blockade failed overall to improve outcomes in highly sensitized patients and prevent the progression to chronic antibody-mediated rejection (ABMR). Similarly, well-conducted studies with C1 inhibitors in sensitized recipients yielded disappointing results so far, in part, because of subtherapeutic dosage used in clinical studies. The emergence of new complement blockers raises hope to significantly reduce the negative effect of ischemia reperfusion, ABMR, and nephropathy recurrence on outcomes after KTx.
    MeSH term(s) Humans ; Kidney Transplantation/adverse effects ; Kidney/pathology ; Transplantation, Homologous ; Complement Activation ; Complement System Proteins ; Isoantibodies ; Ischemia/pathology ; Graft Rejection/prevention & control
    Chemical Substances Complement System Proteins (9007-36-7) ; Isoantibodies
    Language English
    Publishing date 2023-07-13
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.0000000000000192
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  3. Article ; Online: B12 deficiency or thrombotic microangiopathy? The key is in the peripheral smear.

    Alanbari, Nelly / Amiot, Quentin / Zuber, Julien / Boudhabhay, Idris

    EJHaem

    2023  Volume 4, Issue 1, Page(s) 280–281

    Language English
    Publishing date 2023-01-27
    Publishing country United States
    Document type Journal Article
    ISSN 2688-6146
    ISSN (online) 2688-6146
    DOI 10.1002/jha2.644
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  4. Article ; Online: Editorial: Immunogenomics of Solid Organ and Hematopoietic Stem Cell Transplantation.

    Wu, Yongxia / Zuber, Julien / Fu, Jianing

    Frontiers in immunology

    2022  Volume 13, Page(s) 878314

    Language English
    Publishing date 2022-03-16
    Publishing country Switzerland
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.878314
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  5. Article ; Online: Managing immune checkpoint inhibition in transplant recipients.

    Lebbé, Céleste / Biard, Lucie / Delyon, Julie / Zuber, Julien

    The Lancet. Oncology

    2022  Volume 23, Issue 8, Page(s) 969–971

    MeSH term(s) Antineoplastic Agents, Immunological/adverse effects ; CTLA-4 Antigen ; Humans ; Immune Checkpoint Inhibitors ; Transplant Recipients
    Chemical Substances Antineoplastic Agents, Immunological ; CTLA-4 Antigen ; Immune Checkpoint Inhibitors
    Language English
    Publishing date 2022-07-06
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 2049730-1
    ISSN 1474-5488 ; 1470-2045
    ISSN (online) 1474-5488
    ISSN 1470-2045
    DOI 10.1016/S1470-2045(22)00395-3
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  6. Article ; Online: Ravulizumab for the Treatment of aHUS in Adults: Improving Quality of Life.

    Legendre, Christophe / Rebecca-Sberro-Soussan / Zuber, Julien

    Kidney international reports

    2021  Volume 6, Issue 6, Page(s) 1489–1491

    Language English
    Publishing date 2021-05-12
    Publishing country United States
    Document type Editorial
    ISSN 2468-0249
    ISSN (online) 2468-0249
    DOI 10.1016/j.ekir.2021.04.036
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  7. Article ; Online: Complement-driven hemolytic uremic syndrome.

    Leon, Juliette / LeStang, Marie-Bénédicte / Sberro-Soussan, Rebecca / Servais, Aude / Anglicheau, Dany / Frémeaux-Bacchi, Véronique / Zuber, Julien

    American journal of hematology

    2023  Volume 98 Suppl 4, Page(s) S44–S56

    Abstract: Overactivation of the complement alternative pathway drives the pathogenesis of primary atypical hemolytic uremic syndrome (aHUS). Genetically-determined or acquired dysregulation of the complement is frequently identified in patients with aHUS, ... ...

    Abstract Overactivation of the complement alternative pathway drives the pathogenesis of primary atypical hemolytic uremic syndrome (aHUS). Genetically-determined or acquired dysregulation of the complement is frequently identified in patients with aHUS, pregnancy-related hemolytic uremic syndrome (HUS), and severe hypertension-associated HUS. In contrast, it is still unclear whether self-limited complement activation, which frequently occurs in other forms of HUS, provides key mechanistic clues or results from endothelial damage. Development of novel biomarkers is underway to firmly establish complement-driven pathogenesis. C5 blockade therapy has revolutionized the management of aHUS patients, resulting in a halving of the subpopulation under chronic dialysis over the course of a few years. On the other hand, the efficacy of C5 blockade in secondary forms of HUS, as assessed by small and uncontrolled case series, is less compelling and should be investigated through properly designed prospective clinical trials. The increased risk of meningococcal infection, related to C5 inhibition, must be rigorously addressed with suitable prophylaxis. Treatment duration should be determined based on an individualized benefit/risk assessment.
    MeSH term(s) Humans ; Prospective Studies ; Atypical Hemolytic Uremic Syndrome/therapy ; Complement Activation ; Risk Factors ; Biomarkers
    Chemical Substances Biomarkers
    Language English
    Publishing date 2023-01-22
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 196767-8
    ISSN 1096-8652 ; 0361-8609
    ISSN (online) 1096-8652
    ISSN 0361-8609
    DOI 10.1002/ajh.26854
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  8. Article ; Online: Mechanisms of Mixed Chimerism-Based Transplant Tolerance.

    Zuber, Julien / Sykes, Megan

    Trends in immunology

    2017  Volume 38, Issue 11, Page(s) 829–843

    Abstract: Immune responses to allografts represent a major barrier in organ transplantation. Immune tolerance to avoid chronic immunosuppression is a critical goal in the field, recently achieved in the clinic by combining bone marrow transplantation (BMT) with ... ...

    Abstract Immune responses to allografts represent a major barrier in organ transplantation. Immune tolerance to avoid chronic immunosuppression is a critical goal in the field, recently achieved in the clinic by combining bone marrow transplantation (BMT) with kidney transplantation following non-myeloablative conditioning. At high levels of chimerism such protocols can permit central deletional tolerance, but with a significant risk of graft-versus-host (GVH) disease (GVHD). By contrast, transient chimerism-based tolerance is devoid of GVHD risk and appears to initially depend on regulatory T cells (Tregs) followed by gradual, presumably peripheral, clonal deletion of donor-reactive T cells. Here we review recent mechanistic insights into tolerance and the development of more robust and safer protocols for tolerance induction that will be guided by innovative immune monitoring tools.
    MeSH term(s) Animals ; Bone Marrow Transplantation ; Chimerism ; Clonal Deletion ; Humans ; Kidney Transplantation ; T-Lymphocytes, Regulatory/immunology ; Transplantation Chimera ; Transplantation Conditioning/methods ; Transplantation Immunology ; Transplantation Tolerance
    Language English
    Publishing date 2017-08-18
    Publishing country England
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2036831-8
    ISSN 1471-4981 ; 1471-4906
    ISSN (online) 1471-4981
    ISSN 1471-4906
    DOI 10.1016/j.it.2017.07.008
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  9. Article ; Online: De novo thrombotic microangiopathy after kidney transplantation in adults: Interplay between complement genetics and multiple endothelial injury.

    Dessaix, Kathleen / Bontoux, Christophe / Aubert, Olivier / Grünenwald, Anne / Sberro Soussan, Rebecca / Zuber, Julien / Duong Van Huyen, Jean-Paul / Anglicheau, Dany / Legendre, Christophe / Fremeaux Bacchi, Veronique / Rabant, Marion

    American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons

    2024  

    Abstract: De novo thrombotic microangiopathy (dnTMA), after renal transplantation may significantly alter graft outcomes. However, its pathogenesis and the role of complement alternative pathway dysregulation remain elusive. We studied all consecutive adult ... ...

    Abstract De novo thrombotic microangiopathy (dnTMA), after renal transplantation may significantly alter graft outcomes. However, its pathogenesis and the role of complement alternative pathway dysregulation remain elusive. We studied all consecutive adult patients with a kidney allograft biopsy performed between January 2004 and March 2016 displaying dnTMA. Ninety-two patients were included. The median time of occurrence was 166 (IQR 25-811) days. The majority (82.6 %) had TMA localized only in the graft. Calcineurin inhibitor toxicity and antibody-mediated rejection (ABMR) were the 2 most frequent causes (54.3% and 37.0%, respectively). However, etiological factors were multiple in 37% patients. Interestingly, pathogenic variants in the genes of complement alternative pathway were significantly more frequent in the 42 tested patients than in healthy controls (16.7% vs 3.7% respectively, P < .008). The overall graft survival after biopsy was 66.0% at 5 years and 23.4% at 10 years, significantly worse than a matched cohort without TMA. Moreover, graft survival of patients with TMA and ABMR was worse than a matched cohort with ABMR without TMA. The 2 main prognostic factors were a positive C4d staining and a lower estimated glomerular filtration rate at diagnosis. DnTMA is a severe and multifactorial disease, induced by 1 or several endothelium-insulting conditions, mostly calcineurin inhibitor toxicity and ABMR.
    Language English
    Publishing date 2024-02-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2060594-8
    ISSN 1600-6143 ; 1600-6135
    ISSN (online) 1600-6143
    ISSN 1600-6135
    DOI 10.1016/j.ajt.2024.01.029
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  10. Article ; Online: Hot Spot of Complement Factor I Rare Variant p.Ile357Met in Patients With Hemolytic Uremic Syndrome.

    Schwotzer, Nora / Fakhouri, Fadi / Martins, Paula Vieira / Delmas, Yahsou / Caillard, Sophie / Zuber, Julien / Moranne, Olivier / Mesnard, Laurent / Frémeaux-Bacchi, Véronique / El-Sissy, Carine

    American journal of kidney diseases : the official journal of the National Kidney Foundation

    2024  

    Abstract: Atypical hemolytic uremic syndrome (aHUS) is a rare kidney disease due to a dysregulation of the complement alternative pathway. Complement factor I (CFI) negatively regulates the alternative pathway and CFI gene rare variants have been associated to ... ...

    Abstract Atypical hemolytic uremic syndrome (aHUS) is a rare kidney disease due to a dysregulation of the complement alternative pathway. Complement factor I (CFI) negatively regulates the alternative pathway and CFI gene rare variants have been associated to aHUS with a low disease penetrance. We report 10 unrelated cases of HUS associated to a rare CFI variant, p.Ile357Met (c.1071T>G). All patients with isolated p.Ile357Met CFI missense variant were retrospectively identified among patients included between January 2007 and January 2022 in the French HUS Registry. We identified 10 unrelated patients (70% women; median age at HUS diagnosis, 36.5 years) who carry the same rare variant p.Ile357Met in the CFI gene. Seven patients (cases 1-7) presented with aHUS in the native kidney associated with malignant hypertension in 5 patients. None received a C5 inhibitor. Two of these cases occurred in the peripartum period with complete recovery of kidney function, while 5 of these patients reached kidney failure requiring replacement therapy (KFRT). Four patients with KFRT subsequently underwent kidney transplantation. Three later developed C3 glomerulopathy in their kidney graft, but none had aHUS recurrence. Three other patients (cases 8-10) experienced de novo thrombotic microangiopathy after kidney transplantation, precipitated by various triggers. The rare CFI variant p.Ile357Met appears to be a facilitating genetic factor for HUS and for some forms of secondary HUS.
    Language English
    Publishing date 2024-02-28
    Publishing country United States
    Document type Case Reports
    ZDB-ID 604539-x
    ISSN 1523-6838 ; 0272-6386
    ISSN (online) 1523-6838
    ISSN 0272-6386
    DOI 10.1053/j.ajkd.2023.12.021
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