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Effect of Prolactin on Lymphocyte Activation from Systemic Lupus Erythematosus Patients
Author(s) -
CHAVEZRUEDA KARINA,
LEGORRETAHAQUET VICTORIA MA.,
CERVERACASTILLO HERNANDO,
SÁNCHEZ LOURDES,
JARA LUIS JAVIER,
ZENTENO EDGAR,
CHAVEZSANCHEZ LUIS,
BLANCOFAVELA FRANCISCO
Publication year - 2007
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1422.018
Subject(s) - cd154 , peripheral blood mononuclear cell , prolactin , lymphocyte , antibody , endocrinology , medicine , autocrine signalling , immunology , in vitro , receptor , biology , cd40 , hormone , cytotoxic t cell , biochemistry
: The aim was to explore the role of prolactin (PRL) in the lymphocyte activation process in systemic lupus erythematosus (SLE) patients in an in vitro model. Peripheral blood mononuclear cells (PBMCs) were isolated from SLE patients and healthy individuals. The mRNA for PRL and its receptor obtained by standard techniques, with an appropriate primer, were subjected to polymerase chain reaction (PCR) and visualized. The PBMCs were cultured with ( a ) medium alone as a negative control, ( b ) unspecific mitogen as a positive control, ( c ) PRL alone, ( d ) mitogen plus PRL, ( e ) mitogen plus antibody anti‐PRL, and ( f ) mitogen plus a nonrelated antibody. Then CD69 and CD154 were determined by flow cytometry analysis. Twelve inactive and 15 active SLE patients were studied. Twenty‐five percent of the active patients displayed hyperprolactinemia. Under basal conditions CD69 expression was associated with disease activity. The PBMCs activated in vitro were capable of producing and secreting PRL, measured by mRNA and Nb2 assay. In a similar way, the mRNA for the PRL receptor was visualized. Cells from SLE patients cultivated with PRL alone did not display increased CD69 and CD154 expression. The addition of PRL to the unspecific stimulated culture does not have an additive effect. In contrast, the addition of antibodies against PRL in order to block the autocrine PRL resulted in a striking reduction of CD69 and CD154 expression.