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. 1999 Feb;42(2):328-37.
doi: 10.1002/1529-0131(199902)42:2<328::AID-ANR16>3.0.CO;2-#.

Estrogen enhancement of anti-double-stranded DNA antibody and immunoglobulin G production in peripheral blood mononuclear cells from patients with systemic lupus erythematosus

N Kanda  1 , T Tsuchida, K Tamaki
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Free article

Estrogen enhancement of anti-double-stranded DNA antibody and immunoglobulin G production in peripheral blood mononuclear cells from patients with systemic lupus erythematosus

N Kanda et al. Arthritis Rheum. 1999 Feb.
Free article

Abstract

Objective: To study the in vitro effect of estrogen on IgG anti-double-stranded DNA (anti-dsDNA) antibody and total IgG production in peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus (SLE), in order to elucidate its regulatory role in SLE.

Methods: PBMC from SLE patients and normal donors were cultured with 17beta-estradiol (E2). IgG anti-dsDNA antibodies, total IgG, and cytokine activity in the culture supernatants were measured by enzyme-linked immunosorbent assay.

Results: E2 enhanced production of IgG anti-dsDNA antibodies as well as total IgG in PBMC from SLE patients. Anti-dsDNA production in patients with inactive disease was less responsive to E2 than that in patients with active disease. E2 also enhanced total IgG, but not anti-dsDNA, production in the PBMC of normal donors. Antibody production was increased by E2 to a lesser extent in patients' B cells than in their PBMC. Anti-interleukin-10 (anti-IL-10) antibodies partially blocked the E2-induced increase in antibody production in patients' PBMC, but anti-IL-10 had no effect on B cells. E2 increased IL-10 production by patients' monocytes. Exogenous IL-10 acted additively with E2 in increasing antibody production in patients' B cells.

Conclusion: These results suggest that E2 may polyclonally increase the production of IgG, including IgG anti-dsDNA, in SLE patients' PBMC by enhancing B cell activity and by promoting IL-10 production in monocytes. These findings support the involvement of E2 in the pathogenesis of SLE.

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