title: Increased levels of prolactin receptor expression correlate with the early onset of lupus symptoms and increased numbers of transitional-1 B cells after prolactin treatment.
abstract: BACKGROUND
  Prolactin is secreted from the pituitary gland and other organs, as well as by cells such as lymphocytes. Prolactin has an immunostimulatory effect and is associated with autoimmune diseases that are characterised by abnormal B cell activation, such as systemic lupus erythematosus (SLE). Our aim was to determine if different splenic B cell subsets express the prolactin receptor and if the presence of prolactin influences these B cell subsets and correlates with development of lupus.
  
  
  RESULTS
  Using real-time PCR and flow cytometry, we found that different subsets of immature (transitional) and mature (follicular, marginal zone) B cells express different levels of the prolactin receptor and are differentially affected by hyperprolactinaemia. We found that transitional B cells express the prolactin receptor at higher levels compared to mature B cells in C57BL/6 mice and the lupus-prone MRL/lpr and MRL mouse strains. Transitional-1 (T1) B cells showed a higher level of prolactin receptor expression in both MRL/lpr and MRL mice compared to C57BL/6 mice. Hyperprolactinaemia was induced using metoclopramide, which resulted in the development of early symptoms of SLE. We found that T1 B cells are the main targets of prolactin and that prolactin augments the absolute number of T1 B cells, which reflects the finding that this B cell subpopulation expresses the highest level of the prolactin receptor.
  
  
  CONCLUSIONS
  We found that all B cell subsets express the prolactin receptor but that transitional B cells showed the highest prolactin receptor expression levels. Hyperprolactinaemia in mice susceptible to lupus accelerated the disease and increased the absolute numbers of T1 and T3 B cells but not of mature B cells, suggesting a primary effect of prolactin on the early stages of B cell maturation in the spleen and a role of prolactin in B cell differentiation, contributing to SLE onset.
authors.affiliation: Unidad de Investigación Médica en Inmunología, Hospital de Pediatría, CMN Siglo XXI, IMSS, Av Cuauhtemoc 330, Col. Doctores, Mexico, D.F. CP06720, Mexico.
authors.forename: Yadira
authors.initials: Y
authors.lastname: Ledesma-Soto
authors.forename: Francisco
authors.initials: F
authors.lastname: Blanco-Favela
authors.forename: Ezequiel M
authors.initials: EM
authors.lastname: Fuentes-Pananá
authors.forename: Emiliano
authors.initials: E
authors.lastname: Tesoro-Cruz
authors.forename: Rafael
authors.initials: R
authors.lastname: Hernández-González
authors.forename: Lourdes
authors.initials: L
authors.lastname: Arriaga-Pizano
authors.forename: María V
authors.initials: MV
authors.lastname: Legorreta-Haquet
authors.forename: Eduardo
authors.initials: E
authors.lastname: Montoya-Diaz
authors.forename: Luis
authors.initials: L
authors.lastname: Chávez-Sánchez
authors.forename: María E
authors.initials: ME
authors.lastname: Castro-Mussot
authors.forename: Adriana K
authors.initials: AK
authors.lastname: Chávez-Rueda
mesh_terms: D000818:Animals; D016175:B-Lymphocyte Subsets / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D018858:Germinal Center / Q000378:metabolism; D006966:Hyperprolactinemia / Q000276:immunology / Q000378:metabolism; D008180:Lupus Erythematosus, Systemic / Q000235:genetics / Q000276:immunology* / Q000378:metabolism*; D051379:Mice; D008810:Mice, Inbred C57BL; D019463:Mice, Inbred MRL lpr; D054448:Precursor Cells, B-Lymphoid / Q000378:metabolism*; D011388:Prolactin / Q000008:administration & dosage; D011981:Receptors, Prolactin / Q000235:genetics / Q000378:metabolism*; D013154:Spleen / Q000166:cytology / Q000378:metabolism
chemical_list: D011981:Receptors, Prolactin; D011388:Prolactin