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Expression of IL-2R, IL-4R, IL-6R on peripheral blood lymphocytes in systemic lupus erythematosus and correlation with disease activity: a prospective study.
  1. E Y Chan,
  2. C S Lau,
  3. H Zola
  1. Department of Pathology, University of Hong Kong.


    AIMS: To study the expression of interleukin-2 receptor (IL-2R), interleukin-4 receptor (IL-4R) and interleukin-6 receptor (IL-6R) on peripheral blood lymphocytes (PBL) in patients with systemic lupus erythematosus (SLE); to correlate the level of expression of these receptors with SLE disease activity. METHODS: Peripheral blood lymphocytes were studied by a high sensitivity flow cytometry technique using monoclonal antibodies directed against CD25 (IL-2R alpha chain), CD122 (IL-2R beta chain), CD124 (IL-4R), and CD126 (IL-6R). SLE disease activity was scored using the SLE Disease Activity Index, C3 and C4 concentrations, anti-dsDNA level, and absolute lymphocyte count. RESULTS: Compared with normal controls, PBL from patients with SLE had a higher percentage of CD25+ cells (median 20.8% v 16.5%) and a lower percentage of CD122+ cells (median 13.1% v 22.4%). The difference in CD122+ cells was greater in the CD122weak population than the CD122strong (natural killer cell) population. The percentages of CD124+ and CD126+ PBLs in patients with SLE and controls were similar. On CD25+ cells, the relative antigenic level of the IL-2R alpha chain was significantly higher in patients with SLE (median 2.01 v 1.81). The relative antigenic levels of CD122+, CD124+ and CD126+ cells were similar in patients and controls. Neither the percentages nor the relative antigenic levels of all of these cytokine receptors were correlated with any of the parameters of disease activity. CONCLUSION: Lymphocyte activation in patients with SLE was evident from the increase in CD25 expression on PBL, with a reciprocal decrease in CD122 expression. As the expression of IL-2R, IL-4R, IL-6R did not correlate with disease activity, it seems that these cytokine/receptor systems do not play a direct role in disease activation in SLE.

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