title: Prolactin effect on CD69 and CD154 expression by CD4+ cells from systemic lupus erythematosus patients.
abstract: OBJECTIVE
  The aim was to explore the role of prolactine (PRL) in the lymphocyte activation process in active and inactive systemic lupus erythematosus (SLE) patients in an in vitro model.
  
  
  METHODS
  Peripheral blood mononuclear cells (PBMNC) were isolated from SLE patients and healthy individuals. The mRNA for prolactine and its receptor, obtained by standard techniques with an appropriate primer, were subjected to PCR and visualised. The PBMC were cultured with: a) medium alone as a negative control, b) unspecific mitogen as a positive control (PMA-ionomycin for CD154 or concanavalin A for CD69), c) PRL alone, d) mitogen plus PRL, e) mitogen plus antibody anti-PRL (1:50) and f) mitogen plus an unrelated antibody. Then CD69 and CD154 were determined by flow cytometry analysis.
  
  
  RESULTS
  Twelve inactive and 15 active SLE patients were studied. 25% of the active patients displayed hyperprolactinemia. Under basal conditions, CD69 expression was associated with disease activity. In contrast, CD154 did not show this association. The PBMNC activated in vitro were capable of producing and secreting prolactine as measured by mRNA and Nb2 assay. In the same way the mRNA for prolactine receptor was visualized. Cells from SLE patients cultivated with PRL alone did not display increased CD69 or CD154 expression. The addition of PRL to the unspecific stimulated culture did not have an additive effect. In contrast, the addition of antibodies against PRL, in order to block the autocrine prolactine, resulted in a striking reduction in CD69 and CD154 expression.
  
  
  CONCLUSIONS
  PRL is produced and secreted by the immune cell and acts just after the first trigger signal of activation in an autocrine way. The expression of CD69 and CD154 molecules depend partially on the prolactine.
authors.affiliation: Laboratory of Autoimmunity, Immunology Research Unit, Pediatric Hospital, Centro Medico Nacional "Siglo XXI", Instituto Mexicano del Seguro Social (IMSS), México, DF.
authors.forename: K
authors.initials: K
authors.lastname: Chavez-Rueda
authors.forename: M V
authors.initials: MV
authors.lastname: Legorreta-Haquet
authors.forename: H
authors.initials: H
authors.lastname: Cervera-Castillo
authors.forename: L
authors.initials: L
authors.lastname: Sánchez
authors.forename: L J
authors.initials: LJ
authors.lastname: Jara
authors.forename: E
authors.initials: E
authors.lastname: Zenteno
authors.forename: F
authors.initials: F
authors.lastname: Blanco-Favela
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000378:metabolism*; D000945:Antigens, Differentiation, T-Lymphocyte / Q000378:metabolism*; D019898:Autocrine Communication / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D023201:CD40 Ligand / Q000378:metabolism*; D002478:Cells, Cultured; D006801:Humans; D037181:Lectins, C-Type; D008180:Lupus Erythematosus, Systemic / Q000276:immunology* / Q000503:physiopathology*; D008213:Lymphocyte Activation; D008875:Middle Aged; D011388:Prolactin / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis; D011981:Receptors, Prolactin / Q000235:genetics; D000099192:CD69 Antigens
chemical_list: D015703:Antigens, CD; D000945:Antigens, Differentiation, T-Lymphocyte; D023201:CD40 Ligand; D037181:Lectins, C-Type; D011388:Prolactin; D012333:RNA, Messenger; D011981:Receptors, Prolactin; D000099192:CD69 Antigens