Induction of T Regulatory Cells Attenuates Idiopathic Nephrotic Syndrome
Autor: | Ludmilla Le Berre, Jacques Dantal, Jeanne Naulet, Francoise Buzelin, Sarah Bruneau, Jean-Paul Soulillou, Thomas Condamine, Claire Usal, Karine Renaudin, Helga Smit |
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Rok vydání: | 2009 |
Předmět: |
Male
medicine.medical_specialty Adoptive cell transfer Nephrotic Syndrome Receptors Antigen T-Cell urologic and male genital diseases Guanidines T-Lymphocytes Regulatory Nephropathy Recurrence Internal medicine Cyclosporin a medicine Animals IL-2 receptor Glomerulosclerosis Focal Segmental business.industry NF-kappa B Antibodies Monoclonal Glomerulosclerosis FOXP3 General Medicine medicine.disease Adoptive Transfer Kidney Transplantation Rats Transplantation Basic Research Endocrinology Nephrology Cytokines business Nephrotic syndrome Immunosuppressive Agents |
Zdroj: | Journal of the American Society of Nephrology. 20:57-67 |
ISSN: | 1046-6673 |
DOI: | 10.1681/asn.2007111244 |
Popis: | Buffalo/Mna rats spontaneously develop FSGS and nephrotic syndrome as a result of an immune disorder. Similar to some humans with FSGS, the disease recurs after renal transplantation, suggesting the involvement of a circulating factor. Here, we tested the effect of several immunosuppressive treatments on these rats. Although corticosteroids, cyclosporin A, and anti–T cell receptor treatment reduced proteinuria, only the deoxyspergualin derivative LF15-0195 led to a rapid and complete normalization of proteinuria. Furthermore, this compound led to the regression of renal lesions during both the initial disease and posttransplantation recurrence. The frequency of splenic and peripheral CD4+CD25+FoxP3+ T lymphocytes significantly increased with remission. Moreover, the transfer of purified LF15-0195–induced CD4+CD25+ T cells to irradiated Buff/Mna rats significantly reduced their proteinuria compared with the transfer of untreated control cells, suggesting that LF15-0195 induces regulatory T cells that are able to induce regression of rat nephropathy. These data suggest that idiopathic nephrotic syndrome/FSGS disease can be regulated by cellular transfer, but how this regulation leads to the reorganization of the podocyte cytoskeleton remains to be determined. |
Databáze: | OpenAIRE |
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