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• W2021397632 abstract "To the Editor: We read with great interest the recent contribution by Munyentwali et al.1.Munyentwali H. Bouachi K. Audard V. et al.Rituximab is an efficient and safe treatment in adults with steroid-dependent minimal change disease.Kidney Int. 2013; 83: 511-516Abstract Full Text Full Text PDF PubMed Scopus (100) Google Scholar They evaluated the efficacy and safety of rituximab treatment in adult patients with steroid-dependent minimal change nephrotic syndrome (MCNS). They suggested two possible hypotheses: B cells have a potential role in the pathophysiology of MCNS or rituximab stabilizes the cytoskeleton of podocytes. The commentary of Glassock2.Glassock R.J. Therapy of relapsing minimal-change disease in adults: a new approach?.Kidney Int. 2013; 83: 343-345Abstract Full Text Full Text PDF PubMed Scopus (11) Google Scholar shows that more factors could take an important role in the pathogenesis of MCNS such as local factors generated by interleukin (IL)-13, regulatory T cell, and he thought that the T cells affected by B cells might be the source of permeability factor of MCNS. However, we would like to add another possible mechanism of rituximab on steroid-dependent MCNS. Recently, Liu et al.3.Liu L.L. Qin Y. Cai J.F. et al.Th17/Treg imbalance in adult patients with minimal change nephroticsyndrome.Clin Immunol. 2011; 139: 314-320Crossref PubMed Scopus (88) Google Scholar reported about T-helper17 (Th17) cells and regulatory T cells (Treg cells) in patients with MCNS, and they found that IL-17 expression was increased in patients with MCNS with acute renal failure, and that Th17/Treg balance returned to normal after effective corticosteroid therapy.3.Liu L.L. Qin Y. Cai J.F. et al.Th17/Treg imbalance in adult patients with minimal change nephroticsyndrome.Clin Immunol. 2011; 139: 314-320Crossref PubMed Scopus (88) Google Scholar Matsumoto and Kanmatsuse4.Matsumoto K. Kanmatsuse K. Increased urinary excretion of interleukin-17 in nephrotic patients.Nephron. 2002; 91: 243-249Crossref PubMed Scopus (39) Google Scholar also showed that urinary IL-17 was elevated in MCNS, and returned to normal with remission of the disease, and that there was a positive correlation between urinary protein excretion and urinary IL-17. These results suggest that IL-17 could be an important cytokine in the pathogenesis of MCNS. Although not tested in MCNS, there was a study showing the supreme effect of rituximab on Th17 cells and IL-17.5.van de Veerdonk F.L. Lauwerys B. Marijnissen R.J. et al.The anti-CD20 antibody rituximab reduces the Th17 cell response.Arthritis Rheum. 2011; 63: 1507-1516Crossref PubMed Scopus (141) Google Scholar van de Veerdonk et al.5.van de Veerdonk F.L. Lauwerys B. Marijnissen R.J. et al.The anti-CD20 antibody rituximab reduces the Th17 cell response.Arthritis Rheum. 2011; 63: 1507-1516Crossref PubMed Scopus (141) Google Scholar demonstrated that rituximab reduced the number of Th17-positive cells in synovial tissue of rheumatoid arthritis patients, and rituximab reduced IL-17 production induced by Candida albicans in vitro. Therefore, there is a possibility that rituximab might be effective in MCNS by suppression of IL-17, which could be involved in the pathogenesis of MCNS, in addition to the effect of B-cell depletion or cytoskeletal changes in podocytes. However, further studies are necessary to evaluate the exact role of IL-17 in the pathogenesis in MCNS and elucidate the effect of rituximab on molecular and signaling pathways of IL-17. This letter was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (2011-0013789)." @default.
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• W2021397632 title "Could interleukin-17 be a therapeutic target of steroid-dependent minimal change disease?" @default.
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