title: Function of Treg Cells Decreased in Patients With Systemic Lupus Erythematosus Due To the Effect of Prolactin.
abstract: Prolactin has different functions, including cytokine secretion and inhibition of the suppressor effect of regulatory T (Treg) cells in healthy individuals. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by defects in the functions of B, T, and Treg cells. Prolactin plays an important role in the physiopathology of SLE. Our objective was to establish the participation of prolactin in the regulation of the immune response mediated by Treg cells from patients with SLE. CD4CD25CD127 cells were purified using magnetic beads and the relative expression of prolactin receptor was measured. The functional activity was evaluated by proliferation assay and cytokine secretion in activated cells, in the presence and absence of prolactin. We found that both percentage and function of Treg cells decrease in SLE patients compared to healthy individuals with statistical significance. The prolactin receptor is constitutively expressed on Treg and effector T (Teff) cells in SLE patients, and this expression is higher than in healthy individuals. The expression of this receptor differs in inactive and active patients: in the former, the expression is higher in Treg cells than in Teff cells, similar to healthy individuals, whereas there is no difference in the expression between Treg and Teff cells from active patients. In Treg:Teff cell cocultures, addition of prolactin decreases the suppressor effect exerted by Treg cells and increases IFNγ secretion. Our results suggest that prolactin plays an important role in the activation of the disease in inactive patients by decreasing the suppressor function exerted by Treg cells over Teff cells, thereby favoring an inflammatory microenvironment.
authors: From the Unidad de Investigación Médica en Inmunología, Hospital de Pediatría, C.M.N. "Siglo XXI", IMSS, Mexico (L-HMV, C-RK, C-SL, B-FF); Departamento de Reumatología, Clínica 25, IMSS, Mexico (C-CH); Departamento de Bioquímica, Universidad Nacional Autónoma de México, Mexico (Z-GE); Departamento de Reumatología, Hospital de Especialidades, Centro Médico Nacional "Siglo XXI", Mexico (B-FL); Servicio de Reumatología, Hospital General de México, "Dr. Eduardo Liceaga", Mexico (B-VR, Á-HE).
authors: María Victoria
authors: MV
authors: Legorreta-Haquet
authors: Karina
authors: K
authors: Chávez-Rueda
authors: Luis
authors: L
authors: Chávez-Sánchez
authors: Hernando
authors: H
authors: Cervera-Castillo
authors: Edgar
authors: E
authors: Zenteno-Galindo
authors: Leonor
authors: L
authors: Barile-Fabris
authors: Rubén
authors: R
authors: Burgos-Vargas
authors: Everardo
authors: E
authors: Álvarez-Hernández
authors: Francisco
authors: F
authors: Blanco-Favela
mesh_terms: D016022:Case-Control Studies; D002478:Cells, Cultured; D007371:Interferon-gamma / Q000378:metabolism; D008180:Lupus Erythematosus, Systemic / Q000276:immunology*; D011388:Prolactin / Q000502:physiology*; D011981:Receptors, Prolactin / Q000378:metabolism*; D050378:T-Lymphocytes, Regulatory / Q000502:physiology*
chemical_list: D011981:Receptors, Prolactin; D007371:Interferon-gamma; D011388:Prolactin