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Article ; Online: Protection of transplants against antibody-mediated injuries: from xenotransplantation to allogeneic transplantation, mechanisms and therapeutic insights.

Kervella, Delphine / Le Bas-Bernardet, Stéphanie / Bruneau, Sarah / Blancho, Gilles

2022 Volume 13, Page(s) 932242

Abstract: Long-term allograft survival in allotransplantation, especially in kidney and heart transplantation, is mainly limited by the occurrence of antibody-mediated rejection due to anti-Human Leukocyte Antigen antibodies. These types of rejection are difficult ...

Abstract	Long-term allograft survival in allotransplantation, especially in kidney and heart transplantation, is mainly limited by the occurrence of antibody-mediated rejection due to anti-Human Leukocyte Antigen antibodies. These types of rejection are difficult to handle and chronic endothelial damages are often irreversible. In the settings of ABO-incompatible transplantation and xenotransplantation, the presence of antibodies targeting graft antigens is not always associated with rejection. This resistance to antibodies toxicity seems to associate changes in endothelial cells phenotype and modification of the immune response. We describe here these mechanisms with a special focus on endothelial cells resistance to antibodies. Endothelial protection against anti-HLA antibodies has been described
MeSH term(s)	ABO Blood-Group System ; Animals ; Antibodies ; Endothelial Cells ; Graft Rejection/prevention & control ; Kidney Transplantation ; Transplantation, Heterologous ; Transplantation, Homologous
Chemical Substances	ABO Blood-Group System ; Antibodies
Language	English
Publishing date	2022-08-05
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.932242
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Article ; Online: Sterile Pancreas Inflammation during Preservation and after Transplantation.

Kervella, Delphine / Mesnard, Benoît / Prudhomme, Thomas / Bruneau, Sarah / Masset, Christophe / Cantarovich, Diego / Blancho, Gilles / Branchereau, Julien

International journal of molecular sciences

2023 Volume 24, Issue 5

Abstract: The pancreas is very susceptible to ischemia-reperfusion injury. Early graft losses due to pancreatitis and thrombosis represent a major issue after pancreas transplantation. Sterile inflammation during organ procurement (during brain death and ischemia- ... ...

Abstract	The pancreas is very susceptible to ischemia-reperfusion injury. Early graft losses due to pancreatitis and thrombosis represent a major issue after pancreas transplantation. Sterile inflammation during organ procurement (during brain death and ischemia-reperfusion) and after transplantation affects organ outcomes. Sterile inflammation of the pancreas linked to ischemia-reperfusion injury involves the activation of innate immune cell subsets such as macrophages and neutrophils, following tissue damage and release of damage-associated molecular patterns and pro-inflammatory cytokines. Macrophages and neutrophils favor tissue invasion by other immune cells, have deleterious effects or functions, and promote tissue fibrosis. However, some innate cell subsets may promote tissue repair. This outburst of sterile inflammation promotes adaptive immunity activation via antigen exposure and activation of antigen-presenting cells. Better controlling sterile inflammation during pancreas preservation and after transplantation is of utmost interest in order to decrease early allograft loss (in particular thrombosis) and increase long-term allograft survival. In this regard, perfusion techniques that are currently being implemented represent a promising tool to decrease global inflammation and modulate the immune response.
MeSH term(s)	Humans ; Reperfusion Injury ; Kidney Transplantation ; Inflammation ; Pancreas ; Pancreatitis
Language	English
Publishing date	2023-02-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms24054636
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Article ; Online: Role of ICAM-1 in the Adhesion of T Cells to Enteric Glia: Perspectives in the Formation of Plexitis in Crohn's Disease.

Pabois, Julie / Durand, Tony / Le Berre, Catherine / Filippone, Rhiannon T / Noël, Théo / Durieu, Emilie / Bossard, Céline / Bruneau, Sarah / Rolli-Derkinderen, Malvyne / Nurgali, Kulmira / Neunlist, Michel / Bourreille, Arnaud / Neveu, Isabelle / Naveilhan, Philippe

Cellular and molecular gastroenterology and hepatology

2024

Abstract: Background & aims: The presence of myenteric plexitis in the proximal resection margins is a predictive factor of early postoperative recurrence in Crohn's disease. To decipher the mechanisms leading to their formation, T-cell interactions with enteric ... ...

Abstract	Background & aims: The presence of myenteric plexitis in the proximal resection margins is a predictive factor of early postoperative recurrence in Crohn's disease. To decipher the mechanisms leading to their formation, T-cell interactions with enteric neural cells were studied in vitro and in vivo. Methods: T cells close to myenteric neural cells were retrospectively quantified in ileocolonic resections from 9 control subjects with cancer and 20 patients with Crohn's disease. The mechanisms involved in T-cell adhesion were then investigated in co-cultures of T lymphocytes with enteric glial cells (glia). Finally, the implication of adhesion molecules in the development of plexitis and colitis was studied in vitro but also in vivo in Winnie mice. Results: The mean number of T cells close to glia, but not neurons, was significantly higher in the myenteric ganglia of relapsing patients with Crohn's disease (2.42 ± 0.5) as compared with controls (0.36 ± 0.08, P = .0007). Co-culture experiments showed that exposure to proinflammatory cytokines enhanced T-cell adhesion to glia and increased intercellular adhesion molecule-1 (ICAM-1) expression in glia. We next demonstrated that T-cell adhesion to glia was inhibited by an anti-ICAM-1 antibody. Finally, using the Winnie mouse model of colitis, we showed that the blockage of ICAM-1/lymphocyte function-associated antigen-1 (LFA-1) with lifitegrast reduced colitis severity and decreased T-cell infiltration in the myenteric plexus. Conclusions: Our present work argues for a role of glia-T-cell interaction in the development of myenteric plexitis through the adhesion molecules ICAM-1/LFA-1 and suggests that deciphering the functional consequences of glia-T-cell interaction is important to understand the mechanisms implicated in the development and recurrence of Crohn's disease.
Language	English
Publishing date	2024-02-29
Publishing country	United States
Document type	Journal Article
ZDB-ID	2819778-1
ISSN	2352-345X ; 2352-345X
ISSN (online)	2352-345X
ISSN	2352-345X
DOI	10.1016/j.jcmgh.2024.02.016
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Article: MHC Class I Masking to Prevent AMR in a Porcine Kidney Transplantation Model in Alloimmunized Recipients.

Kervella, Delphine / Branchereau, Julien / Prudhomme, Thomas / Nerrière-Daguin, Véronique / Renaudin, Karine / Minault, David / Hervouet, Jérémy / Martinet, Bernard / Bruneau, Sarah / Le Bas-Bernardet, Stéphanie / Blancho, Gilles

Transplantation direct

2023 Volume 9, Issue 6, Page(s) e1490

Abstract: Presensitized patients awaiting a kidney transplant have a lower graft survival and a longer waiting time because of the limited number of potential donors and the higher risk of antibody-mediated rejection (AMR), particularly in the early posttransplant ...

Abstract	Presensitized patients awaiting a kidney transplant have a lower graft survival and a longer waiting time because of the limited number of potential donors and the higher risk of antibody-mediated rejection (AMR), particularly in the early posttransplant period, because of preformed donor-specific antibodies binding major histocompatibility complex (MHC) molecules expressed by the graft endothelium followed by the activation of the complement. Advances in kidney preservation techniques allow the development of ex vivo treatment of transplants. We hypothesized that masking MHC ex vivo before transplantation could help to prevent early AMR in presensitized recipients. We evaluated a strategy of MHC I masking by an antibody during ex vivo organ perfusion in a porcine model of kidney transplantation in alloimmunized recipients. Methods: Through the in vitro calcein-release assay and flow cytometry, we evaluated the protective effect of a monoclonal anti-swine leukocyte antigen class I antibody (clone JM1E3) against alloreactive IgG complement-dependent cytotoxicity toward donor endothelial cells. Kidneys perfused ex vivo with JM1E3 during hypothermic machine perfusion were transplanted to alloimmunized recipients. Results: In vitro incubation of endothelial cells with JM1E3 decreased alloreactive IgG cytotoxicity (mean complement-dependent cytotoxicity index [% of control condition] with 1 µg/mL 74.13% ± 35.26 [calcein assay] and 66.88% ± 33.46 [cytometry]), with high interindividual variability. After transplantation, acute AMR occurred in all recipients on day 1, with signs of complement activation (C5b-9 staining) as soon as 1 h after transplantation, despite effective JM1E3 binding on graft endothelium. Conclusions: Despite a partial protective effect of swine leukocyte antigen I masking with JM1E3 in vitro, ex vivo perfusion of the kidney with JM1E3 before transplantation was not sufficient alone at preventing or delaying AMR in highly sensitized recipients.
Language	English
Publishing date	2023-05-26
Publishing country	United States
Document type	Journal Article
ISSN	2373-8731
ISSN	2373-8731
DOI	10.1097/TXD.0000000000001490
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Article: Calcineurin inhibitors augment endothelial-to-mesenchymal transition by enhancing proliferation in association with cytokine-mediated activation

Woda, Craig B / Bruneau, Sarah / Mak, Anne Linde / Haskova, Zdenka / Liu, Kaifeng / Ghosh, Chandra C / Briscoe, David M

Biochemical and biophysical research communications. 2019 Nov. 19, v. 519, no. 4

2019

Abstract: Calcineurin Inhibitors (CNIs) are routinely used for immunosuppression following solid organ transplantation. However, the prolonged use of these agents lead to organ fibrosis which limits their efficacy. CNIs induce TGFβ expression, which is reported to ...

Abstract	Calcineurin Inhibitors (CNIs) are routinely used for immunosuppression following solid organ transplantation. However, the prolonged use of these agents lead to organ fibrosis which limits their efficacy. CNIs induce TGFβ expression, which is reported to augment endothelial-to-mesenchymal transition (EndMT), but their role in this process is not known. In these studies, we find that the CNIs FK506 and cyclosporine (CsA) are potent to increase endothelial cell (EC) proliferation using established in vitro assays (P < 0.05). Furthermore, using phosphokinase arrays, we find that each CNI activates the MAPK and Akt/mTOR signaling pathways, and that pharmacological inhibition of each pathway targets CNI-induced proliferative responses (P < 0.001). EndMT was evaluated by FACS for N-cadherin and CD31 expression and by qPCR for the expression of α-smooth muscle actin, N-cadherin and Snail. We find that CNIs do not directly induce dedifferentiation, while TGFβ and hypoxia induce EndMT in small numbers of EC. In contrast, the treatment of EC with the inflammatory cytokine TNFα was potent to elicit an EndMT response, and its effects were most notably in EC following proliferation/doubling. Taken together, these observations suggest that CNIs elicit proliferative responses, which enhance EndMT in association with local inflammation. The clinical implications of these findings are that anti-proliferative therapeutics have high potential to target the initiation of this EndMT response.
Keywords	actin ; cadherins ; cyclosporine ; endothelial cells ; fibrosis ; hypoxia ; immunosuppression ; inflammation ; muscles ; organ transplantation ; research
Language	English
Dates of publication	2019-1119
Size	p. 667-673.
Publishing place	Elsevier Inc.
Document type	Article
Note	NAL-AP-2-clean
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2019.09.043
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Article ; Online: Hypomagnesemia, Hypocalcemia, and Tubulointerstitial Nephropathy Caused by Claudin-16 Autoantibodies.

Figueres, Lucile / Bruneau, Sarah / Prot-Bertoye, Caroline / Brideau, Gaëlle / Néel, Mélanie / Griveau, Camille / Cheval, Lydie / Bignon, Yohan / Dimitrov, Jordan / Dejoie, Thomas / Ville, Simon / Kandel-Aznar, Christine / Moreau, Anne / Houillier, Pascal / Fakhouri, Fadi

Journal of the American Society of Nephrology : JASN

2022 Volume 33, Issue 7, Page(s) 1402–1410

Abstract: Background: Chronic hypomagnesemia is commonly due to diarrhea, alcoholism, and drugs. More rarely, it is caused by genetic defects in the effectors of renal magnesium reabsorption.: Methods: In an adult patient with acquired severe hypomagnesemia, ... ...

Abstract	Background: Chronic hypomagnesemia is commonly due to diarrhea, alcoholism, and drugs. More rarely, it is caused by genetic defects in the effectors of renal magnesium reabsorption. Methods: In an adult patient with acquired severe hypomagnesemia, hypocalcemia, tubulointerstitial nephropathy, and rapidly progressing kidney injury, similarities between the patient's presentation and features of genetic disorders of renal magnesium transport prompted us to investigate whether the patient had an acquired autoimmune cause of renal magnesium wasting. To determine if the patient's condition might be explained by autoantibodies directed against claudin-16 or claudin-19, transmembrane paracellular proteins involved in renal magnesium absorption, we conducted experiments with claudin knockout mice and transfected mouse kidney cells expressing human claudin-16 or claudin-19. We also examined effects on renal magnesium handling in rats given intravenous injections of IgG purified from sera from the patient or controls. Results: Experiments with the knockout mice and Conclusions: Pathogenic claudin-16 autoantibodies represent a novel autoimmune cause of specific renal tubular transport disturbances and tubulointerstitial nephropathy. Screening for autoantibodies targeting claudin-16, and potentially other magnesium transporters or channels in the kidney, may be warranted in patients with acquired unexplained hypomagnesemia.
MeSH term(s)	Animals ; Autoantibodies ; Claudins/genetics ; Hypocalcemia ; Immunoglobulin G ; Magnesium ; Mice ; Mice, Knockout ; Nephritis, Interstitial ; Rats
Chemical Substances	Autoantibodies ; Claudins ; Immunoglobulin G ; claudin 16 ; Magnesium (I38ZP9992A)
Language	English
Publishing date	2022-06-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1085942-1
ISSN	1533-3450 ; 1046-6673
ISSN (online)	1533-3450
ISSN	1046-6673
DOI	10.1681/ASN.2022010060
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Article ; Online: Neutrophil-derived extracellular vesicles induce endothelial inflammation and damage through the transfer of miRNAs.

Glémain, Alexandre / Néel, Mélanie / Néel, Antoine / André-Grégoire, Gwennan / Gavard, Julie / Martinet, Bernard / Le Bloas, Rozenn / Riquin, Kevin / Hamidou, Mohamed / Fakhouri, Fadi / Bruneau, Sarah

Journal of autoimmunity

2022 Volume 129, Page(s) 102826

Abstract: The critical role of neutrophils in pathological inflammation, notably in various autoimmune disorders, is currently the focus of renewed interest. Here, we demonstrate for the first time that activation of neutrophils with various inflammatory stimuli ... ...

Abstract	The critical role of neutrophils in pathological inflammation, notably in various autoimmune disorders, is currently the focus of renewed interest. Here, we demonstrate for the first time that activation of neutrophils with various inflammatory stimuli induces the release of extracellular vesicles (EVs) that are internalized by endothelial cells (ECs), thus leading to the transfer of miR-223, miR-142-3p and miR-451 and subsequent endothelial damage. Indeed, while miR-223 has little effect on EC responses, we show that the induced expression of miR-142-3p and miR-451 in ECs results in profound cell damage, especially in inflammatory conditions, characterized by a dramatic increase in cell apoptosis, impaired angiogenic repair responses, and the induction of IL-6, IL-8, CXCL10 and CXCL11 expression. We show that the strong deleterious effect of miR-142-3p may be due in part to its ability to block the activation of ERK1/2 and eNOS-mediated signals in ECs. miR-142-3p also inhibits the expression of RAC1, ROCK2 and CLIC4, three genes that are critical for EC migration and angiogenic responses. Importantly, miR-223, miR-142-3p and miR-451 are markedly increased in kidney biopsies from patients with active ANCA-associated vasculitis, a severe autoimmune disease that is prototypical of a neutrophil-induced microvascular damage. Taken together, our results suggest that miR-142-3p and miR-451 released in EVs by activated neutrophils can target EC to trigger an inflammatory cascade and induce direct vascular damage, and that therapeutic strategies based on the inhibition of these miRNAs in ECs will have implications for neutrophil-mediated inflammatory diseases.
MeSH term(s)	Chloride Channels/metabolism ; Endothelial Cells/metabolism ; Extracellular Vesicles/metabolism ; Humans ; Inflammation/metabolism ; MicroRNAs/genetics ; Neutrophils/metabolism
Chemical Substances	CLIC4 protein, human ; Chloride Channels ; MicroRNAs
Language	English
Publishing date	2022-04-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639452-8
ISSN	1095-9157 ; 0896-8411
ISSN (online)	1095-9157
ISSN	0896-8411
DOI	10.1016/j.jaut.2022.102826
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Article ; Online: Calcineurin inhibitors augment endothelial-to-mesenchymal transition by enhancing proliferation in association with cytokine-mediated activation.

Woda, Craig B / Bruneau, Sarah / Mak, Anne Linde / Haskova, Zdenka / Liu, Kaifeng / Ghosh, Chandra C / Briscoe, David M

Biochemical and biophysical research communications

2019 Volume 519, Issue 4, Page(s) 667–673

Abstract	Calcineurin Inhibitors (CNIs) are routinely used for immunosuppression following solid organ transplantation. However, the prolonged use of these agents lead to organ fibrosis which limits their efficacy. CNIs induce TGFβ expression, which is reported to augment endothelial-to-mesenchymal transition (EndMT), but their role in this process is not known. In these studies, we find that the CNIs FK506 and cyclosporine (CsA) are potent to increase endothelial cell (EC) proliferation using established in vitro assays (P < 0.05). Furthermore, using phosphokinase arrays, we find that each CNI activates the MAPK and Akt/mTOR signaling pathways, and that pharmacological inhibition of each pathway targets CNI-induced proliferative responses (P < 0.001). EndMT was evaluated by FACS for N-cadherin and CD31 expression and by qPCR for the expression of α-smooth muscle actin, N-cadherin and Snail. We find that CNIs do not directly induce dedifferentiation, while TGFβ and hypoxia induce EndMT in small numbers of EC. In contrast, the treatment of EC with the inflammatory cytokine TNFα was potent to elicit an EndMT response, and its effects were most notably in EC following proliferation/doubling. Taken together, these observations suggest that CNIs elicit proliferative responses, which enhance EndMT in association with local inflammation. The clinical implications of these findings are that anti-proliferative therapeutics have high potential to target the initiation of this EndMT response.
MeSH term(s)	Animals ; CHO Cells ; Cadherins/metabolism ; Calcineurin Inhibitors/pharmacology ; Cell Proliferation/drug effects ; Cells, Cultured ; Cricetinae ; Cricetulus ; Cyclosporine/pharmacology ; Epithelial-Mesenchymal Transition/drug effects ; Human Umbilical Vein Endothelial Cells/drug effects ; Human Umbilical Vein Endothelial Cells/metabolism ; Human Umbilical Vein Endothelial Cells/physiology ; Humans ; Signal Transduction/drug effects ; Tacrolimus/pharmacology ; Tumor Necrosis Factor-alpha/pharmacology
Chemical Substances	Cadherins ; Calcineurin Inhibitors ; Tumor Necrosis Factor-alpha ; Cyclosporine (83HN0GTJ6D) ; Tacrolimus (WM0HAQ4WNM)
Language	English
Publishing date	2019-09-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2019.09.043
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Article ; Online: New insights into the pathophysiology of idiopathic nephrotic syndrome.

Bruneau, Sarah / Dantal, Jacques

Clinical immunology (Orlando, Fla.)

2009 Volume 133, Issue 1, Page(s) 13–21

Abstract: Corticoresistant idiopathic nephrotic syndrome (INS) is a glomerulopathy of unknown etiology whose original aspect is its recurrence after kidney transplantation in 30 to 50% of patients with end-stage renal disease. This suggests the involvement of ... ...

Abstract	Corticoresistant idiopathic nephrotic syndrome (INS) is a glomerulopathy of unknown etiology whose original aspect is its recurrence after kidney transplantation in 30 to 50% of patients with end-stage renal disease. This suggests the involvement of circulating factors that would alter the glomerular filtration barrier, but whose nature remains elusive. Although a T cell immune origin has been suggested, the actual role of these cells in INS recurrence is still unclear. Here we present an 8-year-old patient with corticoresistant INS who developed a recurrence of her initial disease after kidney transplantation. Rituximab therapy was proposed 11 months after transplantation; although no immediate effect was induced, a slow but persistent decrease in proteinuria began a few months after Rituximab infusions despite cessation of plasma exchanges and steroid therapy. The pathophysiology of INS and the putative mechanisms of action of Rituximab are discussed.
MeSH term(s)	Adolescent ; Adult ; Antibodies, Monoclonal/therapeutic use ; Antibodies, Monoclonal, Murine-Derived ; Child ; Female ; Humans ; Immunologic Factors/therapeutic use ; Kidney Failure, Chronic/surgery ; Kidney Transplantation ; Male ; Middle Aged ; Nephrotic Syndrome/drug therapy ; Nephrotic Syndrome/immunology ; Postoperative Complications/drug therapy ; Postoperative Complications/immunology ; Recurrence ; Rituximab ; T-Lymphocyte Subsets/immunology ; Treatment Outcome
Chemical Substances	Antibodies, Monoclonal ; Antibodies, Monoclonal, Murine-Derived ; Immunologic Factors ; Rituximab (4F4X42SYQ6)
Language	English
Publishing date	2009-10
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1459903-x
ISSN	1521-7035 ; 1521-6616
ISSN (online)	1521-7035
ISSN	1521-6616
DOI	10.1016/j.clim.2009.03.532
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Article ; Online: DEPTOR modulates activation responses in CD4

Wedel, Johannes / Bruneau, Sarah / Liu, Kaifeng / Kong, Sek Won / Sage, Peter T / Sabatini, David M / Laplante, Mathieu / Briscoe, David M

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

2018 Volume 19, Issue 1, Page(s) 77–88

Abstract: DEPTOR is an evolutionarily conserved cell-intrinsic binding partner of mTOR that functions as a negative regulator of signaling responses. In this study, we show that DEPTOR is expressed within ... ...

Abstract	DEPTOR is an evolutionarily conserved cell-intrinsic binding partner of mTOR that functions as a negative regulator of signaling responses. In this study, we show that DEPTOR is expressed within CD4
MeSH term(s)	Animals ; Forkhead Transcription Factors/metabolism ; Glucose/metabolism ; Graft Rejection ; Graft Survival/drug effects ; Heart Transplantation ; Intracellular Signaling Peptides and Proteins/metabolism ; Male ; Methylation ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Transgenic ; Oxygen/chemistry ; Phosphorylation ; Skin Transplantation ; T-Lymphocytes, Regulatory/cytology ; Transplantation, Homologous
Chemical Substances	Forkhead Transcription Factors ; Foxp3 protein, mouse ; Intracellular Signaling Peptides and Proteins ; deptor protein, mouse ; Glucose (IY9XDZ35W2) ; Oxygen (S88TT14065)
Language	English
Publishing date	2018-08-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2060594-8
ISSN	1600-6143 ; 1600-6135
ISSN (online)	1600-6143
ISSN	1600-6135
DOI	10.1111/ajt.14995
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