NDLI: Regulatory T cells improve nephrocalcinosis but not dystrophic cardiac calcinosis in DBA/2 mice.

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Regulatory T cells improve nephrocalcinosis but not dystrophic cardiac calcinosis in DBA/2 mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Kirsch, Alexander H. Smaczny, Nicole Riegelbauer, Viktoria Sedej, Simon Hofmeister, Alexander Stojakovic, Tatjana Goessler, Walter Brodmann, Marianne Pilger, Ernst Rosenkranz, Alexander R. Eller, Kathrin Eller, Philipp
Description	Country affiliation: Austria Author Affiliation: Kirsch AH ( Clinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, Graz, Austria.)
Abstract	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-CD3É 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.
File Format	HTM / HTML
ISSN	00029440
Issue Number	2
Volume Number	183
e-ISSN	15252191
Journal	The American Journal of Pathology
Language	English
Publisher	Elsevier (on behalf of the American Society for Investigative Pathology)
Publisher Date	2013-08-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Durapatite Phosphates Research Support, Non-u.s. Gov't Nephrocalcinosis Toxicity Antigens, Cd3 Discipline Pathology Pharmacology T-lymphocytes, Regulatory Antibodies, Monoclonal Metabolism Chemically Induced Journal Article Phenotype Immunology Animals Lymphopenia Cardiomyopathies Female Mice, Inbred Dba Physiology Mice Vascular Calcification
Content Type	Text
Resource Type	Article
Subject	Pathology and Forensic Medicine

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