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SAT0109 Expression of bcl-2 in juvenile chronic arthritis
  1. E Tuszkiewicz-Misztal1,
  2. A Bojarska-Junak2,
  3. P Krawczyk2,
  4. J Roliñski2,
  5. V Opoka-Winiarska1
  1. 1Department of Paediatrics, Pulmonary Diseases and Rheumatology
  2. 2Department of Clinical Immunology, Medical University, Lublin, Poland

Abstract

Background The aim of this study was to investigate the relationship between levels of molecules regulating of apoptosis in T lymphocytes and the clinical manifestation of juvenile chronic arthritis (JCA).

Objectives Apoptosis is involved in the regulation of an immune response to foreign and autoantigens. We determined the expression of Bcl-2 mitochondrial oncoprotein, which inhibit apoptosis, in different subtypes of lymphocytes obtained from peripheral blood from healthy children (n = 14, age:12,4 ± 5,4) and JCA patients with pauciarticular onset (n = 17, age: 12,2 ± 3,8) and polyarticular onset (n = 30, age: 11,8 ± 3,2).

Methods All samples were analysed using monoclonal antibodies and flow cytometry technique.

Results Peripheral blood T lymphocytes from patients with pauciarticular onset JCA expressed a significantly lower amount of the Bcl-2 protein than T lymphocytes from patients with polyarticular onset JCA (p < 0,01) and healthy children (p < 0,05). This differences concerned both CD4+ and CD8+ T cells but CD4+ lymphocytes expressed significantly (p < 0,05) lower level of Bcl-2 protein in comparison with CD8+ cells in patients with polyarticular onset JCA. There were no correlations between the expression of Bcl-2 and the age of children in all subgroup of patients. There was significant positive correlation (R = 0,562, p < 0,05) between the percentage of T lymphocytes with receptor for IL-2 (CD25) and expression of Bcl-2 protein in T cells in children with pauciarticular onset JCA.

Conclusion Our data supported the notion that disturbances in T cell apoptosis may play a role in the immunopathological processes leading to clinical manifestation of JCA, These data suggest also that both polyarticular onset and pauciarticular onset JCA have different pathogenesis and probably distinct aetiologies.

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