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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Medicine+(Baltimore)
2016 ; 95
(5
): e2384
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Function of Treg Cells Decreased in Patients With Systemic Lupus Erythematosus
Due To the Effect of Prolactin
#MMPMID26844452
Legorreta-Haquet MV
; Chávez-Rueda K
; Chávez-Sánchez L
; Cervera-Castillo H
; Zenteno-Galindo E
; Barile-Fabris L
; Burgos-Vargas R
; Álvarez-Hernández E
; Blanco-Favela F
Medicine (Baltimore)
2016[Feb]; 95
(5
): e2384
PMID26844452
show ga
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 IFN? 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.