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Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Arthritis+Rheumatol 2016 ; 68 (7): 1758-68 Nephropedia Template TP
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Next Generation Sequencing Reveals Restriction and Clonotypic Expansion of Regulatory T Cells in Juvenile Idiopathic Arthritis #MMPMID26815131
Henderson LA; Volpi S; Frugoni F; Janssen E; Kim S; Sundel RP; Dedeoglu F; Lo MS; Hazen MM; Son MB; Mathieu R; Zurakowski D; Yu N; Lebedeva T; Fuhlbrigge RC; Walter JE; Lee YN; Nigrovic PA; Notarangelo LD
Arthritis Rheumatol 2016[Jul]; 68 (7): 1758-68 PMID26815131show ga
Objective: Regulatory T (Treg) cell mediated suppression of effector T (Teff) cells is impaired in juvenile idiopathic arthritis (JIA); however, the basis for this dysfunction is incompletely understood. Animal models of autoimmunity and immunodeficiency demonstrate that a diverse Treg repertoire is essential to maintain Treg cell function. We therefore employed next generation sequencing to investigate the Treg and Teff repertoires in JIA. Methods: Treg (CD4+CD25+CD127lo) and Teff (CD4+CD25?) cells were isolated from peripheral blood and synovial fluid obtained from JIA patients, controls, and children with Lyme arthritis. Treg cell function was measured in suppressive assays. The T cell receptor ? chain (TRB) was amplified by multiplex PCR, and amplicons were sequenced with the Illumina HiSeq platform. Data was analyzed using ImmunoSEQ?, International ImMunoGeneTics system, and the Immunoglobulin Analysis Tools. Results: Compared to controls, the JIA peripheral blood Treg repertoire was restricted and clonotypic expansions were found in both blood and synovial fluid Treg cells. Skewed usage and pairing of TRB variable and joining genes, including overuse of gene segments that have been associated with other autoimmune conditions, was observed. JIA patients shared a substantial portion of synovial fluid Treg clonotypes that were private to JIA and not identified in Lyme arthritis. Conclusions: Our data identified restriction and clonotypic expansions in the JIA Treg repertoire with sharing of Treg clonotypes across arthritis patients. These findings suggest that abnormalities in the Treg repertoire, possibly engendered by shared antigenic triggers, may contribute to disease pathogenesis in JIA.