Increased interferon‐gamma (IFN‐γ), IL‐10 and decreased IL‐4 mRNA expression in peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus (SLE)

Cytokines are important regulators of lymphocyte function in SLE. However, the profile of Th1 and Th2 cytokines produced by circulating lymphocytes in human SLE has not been clearly elucidated. The aim of the present study was to characterize the gene expressions of the Th1‐type cytokine IFN‐γ, and...

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Published inClinical and experimental immunology Vol. 122; no. 3; pp. 464 - 470
Main Authors Csiszár, A., Nagy, GY, Gergely, P., Pozsonyi, T., Pócsik, É.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.12.2000
Blackwell
Oxford University Press
Blackwell Science Inc
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Summary:Cytokines are important regulators of lymphocyte function in SLE. However, the profile of Th1 and Th2 cytokines produced by circulating lymphocytes in human SLE has not been clearly elucidated. The aim of the present study was to characterize the gene expressions of the Th1‐type cytokine IFN‐γ, and the Th2‐type cytokines IL‐10 and IL‐4 in PBMC of 15 patients with SLE and 10 healthy individuals by a semiquantitative reverse transcriptase polymerase chain reaction (RT‐PCR). Our results showed that expression of IFN‐γ (P = 0·0004) and IL‐10 (P = 0·002) transcripts were significantly increased in PBMC of patients with SLE compared with healthy controls. By contrast, expression of IL‐4 transcripts in PBMC of patients with SLE was significantly decreased compared with the healthy controls (P = 0·0008). Primary sources of IL‐10 were B cells and monocytes, with variable contribution of T cells as detected in various fractions of PBMC of patients with SLE (P = 0·049). These findings support the hypothesis that the enhanced production of IFN‐γ by mononuclear cells may trigger inflammatory responses, together with the enhanced production of IL‐10 resulting in autoantibody production by B cells in human SLE.
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ISSN:0009-9104
1365-2249
DOI:10.1046/j.1365-2249.2000.01369.x