title: Differential expression of estrogen receptors in women with systemic lupus erythematosus.
abstract: OBJECTIVE
  Systemic lupus erythematosus (SLE) is an autoimmune disease primarily affecting women. T cell activation markers (calcineurin, CD154) increase in SLE T cells cultured with estradiol 17-beta. Biological effects of estradiol are mediated through 2 receptor proteins, estrogen receptor-alpha (ER-alpha) and estrogen receptor-beta (ER-beta). We compared the amount of estrogen receptor subtypes in T cells and measured the ability of receptor agonist-specific ligands to activate marker gene expression.
  
  
  METHODS
  T cells were isolated from 22 female patients with SLE and 17 control women. The amount of ER subtypes was measured by immunoblotting. Some T cells were cultured with ER-alpha or ER-beta-specific agonists. Receptor activation was measured by increased expression of the T cell activation markers CD154 and calcineurin.
  
  
  RESULTS
  Although the amount of ER-alpha appeared to be less in SLE T cells than in control T cells, the difference was not statistically significant (p = 0.081). The quantity of ER-beta was similar in SLE and control T cells. The expression of ER-alpha or ER-beta was independent of menstrual cycle phase, age, or SLE disease activity. Calcineurin and CD154 expression increased in SLE T cells cultured in medium containing ER-alpha and ER-beta agonists.
  
  
  CONCLUSIONS
  These data indicate that both ER subtypes activate calcineurin and CD154 in SLE but not in normal T cells. Variation in the amount of ER-alpha in SLE T cells suggests this receptor subtype participates in the sensitivity of SLE T cells to estrogen.
authors.affiliation: Department of Biology, Pittsburg State University, Kansas 66762, USA. vrider@pittstate.edu
authors.forename: Virginia
authors.initials: V
authors.lastname: Rider
authors.forename: Xiaolan
authors.initials: X
authors.lastname: Li
authors.forename: Greg
authors.initials: G
authors.lastname: Peterson
authors.forename: Joyce
authors.initials: J
authors.lastname: Dawson
authors.forename: Bruce F
authors.initials: BF
authors.lastname: Kimler
authors.forename: Nabih I
authors.initials: NI
authors.lastname: Abdou
mesh_terms: D000199:Actins / Q000494:pharmacology; D000328:Adult; D015415:Biomarkers / Q000378:metabolism; D015153:Blotting, Western; D023201:CD40 Ligand / Q000378:metabolism; D019703:Calcineurin / Q000378:metabolism; D002478:Cells, Cultured; D047628:Estrogen Receptor alpha / Q000819:agonists / Q000378:metabolism*; D047629:Estrogen Receptor beta / Q000819:agonists / Q000378:metabolism*; D005260:Female; D006304:Health Status; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000276:immunology / Q000378:metabolism* / Q000503:physiopathology; D008213:Lymphocyte Activation / Q000187:drug effects; D008597:Menstrual Cycle / Q000276:immunology / Q000378:metabolism; D008875:Middle Aged; D012720:Severity of Illness Index; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*
chemical_list: D000199:Actins; D015415:Biomarkers; D047628:Estrogen Receptor alpha; D047629:Estrogen Receptor beta; D023201:CD40 Ligand; D019703:Calcineurin