دورية أكاديمية
A CD31-Derived Peptide Prevents the Development of Antibody-Mediated Lesions in a Rat Model of Aortic Allograft
| العنوان: | A CD31-Derived Peptide Prevents the Development of Antibody-Mediated Lesions in a Rat Model of Aortic Allograft |
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| المؤلفون: | Sannier, Aurélie, Stroumza, Nathaniel, Atlan, Michaël, Even, Guillaume, Guedj, Kevin, Sénémaud, Jean Nicolas, Coscas, Raphaël, Caligiuri, Giuseppina, Nicoletti, Antonino |
| المساهمون: | Institut National de la Santé et de la Recherche Médicale (INSERM), Département d'Anatomo-Pathologie Hôpital Bichat, AP-HP - Hôpital Bichat - Claude Bernard Paris, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), CHU Tenon AP-HP, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Sorbonne Université (SU), Université de Versailles Saint-Quentin-en-Yvelines (UVSQ), Hôpital Ambroise Paré AP-HP, Agence Nationale de la Recherche, ANR: ANR-16-CE17-0007, This work was supported by the Agence Nationale de la Recherche (ANR-16-CE17-0007) and the Soci?t? Francophone de Transplantation (grant to Aur?lie Sannier)., ANR-16-CE17-0007,PETTAR,Ciblage de PECAM-1 pour la prévention et le traitement du rejet humoral en transplantation d'organe(2016) |
| المصدر: | ISSN: 0041-1345. |
| بيانات النشر: | HAL CCSD Elsevier |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | [SDV]Life Sciences [q-bio] |
| الوصف: | International audience ; Background: Antibody-mediated rejection (AMR) is a major cause of graft loss. The development of donor-specific antibodies (DSAs) directed against the allogeneic HLA molecules expressed by the graft also leads to accelerated arteriosclerosis. CD31 is a protein expressed on endothelial and immune cells, ensuring homeostasis at this interface. When strong immune stimulation occurs, the regulatory function of CD31 is lost owing to cleavage of its extracellular portion. P8RI, a synthetic peptide that binds to the ectodomain of CD31, is able to restore the CD31 immunomodulatory function. In this study, we hypothesized that CD31 could represent an attractive molecular target in AMR and investigated whether P8RI could prevent the development of vascular antibody-mediated lesions. Materials and methods: A rat model of orthotopic aortic allograft was used, and P8RI was administered for 28 days. Circulating DSAs were quantified to assess the alloimmune humoral response, and histologic and immunohistochemical analyses of aortic allografts were performed to estimate antibody-mediated lesions in the allograft. Results: Aorta-allografted rats receiving P8RI developed fewer DSAs than control animals (mean fluorescence intensity 344 vs 741). The density of nuclei in the media (3.4 x 10-5 vs 2.2 x 10-5 nuclei/px2) and media surface area (2.33 x 106 vs 2.02 x 106 px2) were higher in animals treated with P8RI than in control animals. Conclusions: These data support a therapeutic potential for molecules able to restore the CD31 signaling to fight AMR. P8RI, an agonist synthetic peptide targeting CD31, might prevent DSA production and have a beneficial effect in limiting arterial antibody-mediated lesions. CD31 agonists may become therapeutic tools to prevent and treat solid organ transplant arteriosclerosis. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| العلاقة: | info:eu-repo/semantics/altIdentifier/pmid/33549347; hal-03171228; https://hal.science/hal-03171228Test; https://hal.science/hal-03171228/documentTest; https://hal.science/hal-03171228/file/S004113452100004X.pdfTest; PII: S0041-1345(21)00004-X; PUBMED: 33549347 |
| DOI: | 10.1016/j.transproceed.2021.01.003 |
| الإتاحة: | https://doi.org/10.1016/j.transproceed.2021.01.003Test https://hal.science/hal-03171228Test https://hal.science/hal-03171228/documentTest https://hal.science/hal-03171228/file/S004113452100004X.pdfTest |
| حقوق: | http://creativecommons.org/licenses/by-ncTest/ ; info:eu-repo/semantics/OpenAccess |
| رقم الانضمام: | edsbas.A0F3016C |
| قاعدة البيانات: | BASE |
| DOI: | 10.1016/j.transproceed.2021.01.003 |
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