Prevalence of Fc‐gammaR chain expression in CD4+ T cells of patients with systemic lupus erythematosus

L Butkiewicz, S Duriagin, R Laddach… - Scandinavian journal …, 2005 - Taylor & Francis
L Butkiewicz, S Duriagin, R Laddach, H Chwalinska‐Sadowska, PP Jagodzinski
Scandinavian journal of rheumatology, 2005Taylor & Francis
Objective: To determine the upregulation of transcript and protein levels of the T cell receptor
(TCR)/CD3‐Fc‐gammaR chain in CD4+ T cells of systemic lupus erythematosus (SLE)
patients with different clinical disease activity scored on the SLE Disease Activity Index
(SLEDAI) scale. Methods: CD4+ cells were isolated by the positive biomagnetic separation
technique. Quantitative analysis of Fc‐gammaR cDNA was carried out by using the real‐
time quantitative polymerase chain reaction (RQ‐PCR) SYBR Green I system. Protein levels …
Objective: To determine the upregulation of transcript and protein levels of the T cell receptor (TCR)/CD3‐Fc‐gammaR chain in CD4+ T cells of systemic lupus erythematosus (SLE) patients with different clinical disease activity scored on the SLE Disease Activity Index (SLEDAI) scale.
Methods: CD4+ cells were isolated by the positive biomagnetic separation technique. Quantitative analysis of Fc‐gammaR cDNA was carried out by using the real‐time quantitative polymerase chain reaction (RQ‐PCR) SYBR Green I system. Protein levels of Fc‐gammaR in CD4+ T cells were determined by Western blotting analysis.
Results: We observed significantly higher transcript and protein levels of the Fc‐gammaR chain in CD4+ T cells of SLE patients (n = 45) than in healthy individuals (n = 26). The increase in Fc‐gammaR expression was observed in 97.8% of SLE patients. Spearman statistical analysis suggests that the protein level of Fc‐gammaR in CD4+ T cells may correlate with SLE activity scored by the SLEDAI scale (R = 0.556, p<0.00006, respectively).
Conclusion: The high prevalence of the Fc‐gammaR chain in CD4+ T cells of SLE patients may indicate an important role for this molecule in the pathogenesis of SLE.
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