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AB0203 The role of estrogens on the production of IL-21 in patients with systemic lupus erythematosus
  1. J. Lee1,
  2. S.M. Jung1,
  3. J.H. Lee1,
  4. J.M. Kim1,
  5. M.-L. Cho2,
  6. S.-K. Kwok1,
  7. J.H. Ju1,
  8. K.-S. Park1,
  9. S.-H. Park1,
  10. H.-Y. Kim1
  1. 1Internal medicine, division of rheumatology, The catholic university of Korea, Seoul St.Mary’s hospital
  2. 2Rheumatism Research Center (RhRC) Catholic Institute of Medical Sciences The Catholic University of Korea, Seoul, Korea, Republic Of

Abstract

Background Systemic lupus erythematosus (SLE) is an autoimmune disease in which various organs and tissues are damaged through abnormal immune responses mediated by tissue-binding autoantibodies. Though, the exact pathogenic mechanism is not clearly elucidated, estrogens are thought to play an important role because over 90% of SLE patients are women. IL-21 is an important cytokine which is produced by T cells, especially Th17 and induces B cell activation. Thus, it has been suggested that IL-21 plays a critical role in the pathogenesis of autoimmune diseases.

Objectives We investigated the effect of estrogens on the production of IL-21 and subsequent B cell activation in SLE patients.

Methods Peripheral blood mononuclear cells (PBMCs) were obtained from peripheral blood of SLE patients and healthy controls. CD4+ T cells, non CD4+ T cells, B cells were isolated using micro beads. The expression of IL-21 and its receptors was assessed by ELISA (serum) and real time PCR (PBMCs, CD4+ cells). The level of immunoglobulin G secreted by activated B cells were measured with specific ELISA.

Results The expression of IL-21 and its receptors in serum, PBMC, and CD4+ T cells was higher in patients with SLE compared to healthy controls. The production of IL-21 was increased when the cells are stimulated with estrogen in dose- and time- dependent manners. IL-21 production was decreased in the presence of MAP kinase (MEK, p38, JNK) inhibitors. B cells of healthy controls showed an increased antibody production when they were co-cultured with estrogen-stimulated CD4+ T cells of patients with SLE. IL-21 antibodies suppressed the increased antibody production of the co-culture systems.

Conclusions This study revealed a possible role of estrogens in the pathogenesis of SLE. Estrogens increase the production of IL-21 by activating CD4+ T cells via MAP kinase dependent pathways in SLE patients.

Disclosure of Interest None Declared

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