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SHR Neuro Krebs Kardio Lipid Stoffw Microb

Kirsch, AH; Smaczny, N; Riegelbauer, V; Sedej, S; Hofmeister, A; Stojakovic, T; Goessler, W; Brodmann, M; Pilger, E; Rosenkranz, AR; Eller, K; Eller, P.
Regulatory T cells improve nephrocalcinosis but not dystrophic cardiac calcinosis in DBA/2 mice.
Am J Pathol. 2013; 183(2):382-390 Doi: 10.1016/j.ajpath.2013.04.012 [OPEN ACCESS]
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Führende Autor*innen der Med Uni Graz
Eller Philipp
Kirsch Alexander
Co-Autor*innen der Med Uni Graz
Brodmann Marianne
Eller Kathrin
Hofmeister Alexander
Koter Nicole
Pilger Ernst
Rosenkranz Alexander
Sedej Simon
Stojakovic Tatjana

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Nephrocalcinosis is characterized by aberrant deposition of calcium in the kidneys and is seen in phosphate nephropathy, primary hyperparathyroidism, and distal renal tubular acidosis. To further evaluate the specific pathophysiologic role of T cells in ectopic calcification, we used DBA/2 mice that are prone to develop nephrocalcinosis and dystrophic cardiac calcinosis. Female DBA/2 mice were depleted of T cells (n = 10) or regulatory T cells (Tregs) (n = 15) using either an anti-CD3ɛ or an anti-CD25 monoclonal antibody and compared with isotype-treated controls (n = 9; n = 15), respectively. After this immunomodulation, the DBA/2 mice were given a high-phosphate diet for 9 days and the degree of calcification was assessed by microcomputed tomography. Successful depletion was confirmed by flow cytometry of splenocytes. In DBA/2 mice, the high-phosphate diet induced a phenotype of nephrocalcinosis and dystrophic cardiac calcinosis. T-cell depletion significantly increased renal calcification in microcomputed tomography (P = 0.022). Concordantly, Treg depletion significantly deteriorated acute phosphate nephropathy (P = 0.039) and was associated with a significantly increased mortality rate (P = 0.004). Immunomodulation had no impact on the amount of cardiac calcification. Semiquantitative histopathologic evaluations with Alizarin Red staining independently confirmed the respective radiologic measurements. In summary, our data suggest a pivotal role of T cells, particularly Tregs, in the progression of nephrocalcinosis and emphasize the fact that inflammation deteriorates the outcome in acute phosphate nephropathy. Copyright © 2013 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Antibodies, Monoclonal - pharmacology
Antigens, CD3 - immunology
Cardiomyopathies - chemically induced
Cardiomyopathies - immunology
Durapatite - metabolism
Female -
Lymphopenia - chemically induced
Lymphopenia - immunology
Mice -
Mice, Inbred DBA -
Nephrocalcinosis - chemically induced
Nephrocalcinosis - immunology
Phenotype -
Phosphates - toxicity
T-Lymphocytes, Regulatory - physiology
Vascular Calcification - chemically induced
Vascular Calcification - immunology

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