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Prolactin down-regulates CD4+CD25hiCD127low/- regulatory T cell function in humans.

M V Legorreta-Haquet1, K Chávez-Rueda, E Montoya-Díaz

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Journal of Molecular Endocrinology
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Summary

Prolactin (PRL) regulates immune responses. This study found that prolactin inhibits regulatory T (Treg) cell function and promotes Th1 cytokine secretion, impacting T cell activation and differentiation.

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Area of Science:

  • Immunology
  • Endocrinology
  • Cell Biology

Background:

  • Prolactin (PRL) is known to influence immune responses, including T cell activation, differentiation, and proliferation.
  • The specific mechanisms by which PRL regulates regulatory T (Treg) cells remain largely unelucidated.
  • Understanding PRL's role in Treg cell function is crucial for comprehending immune system regulation.

Purpose of the Study:

  • To investigate the role of prolactin (PRL) in the function of regulatory T (Treg) cells.
  • To determine the expression patterns of PRL and its receptor in Treg and effector T (Teff) cells.
  • To assess the impact of PRL on Treg cell-mediated suppression and cytokine secretion.

Main Methods:

  • Quantified PRL and PRL receptor expression in human Treg and Teff cells.
  • Assessed Treg cell functional activity, including proliferation and cytokine secretion, in response to anti-CD3/CD28 stimulation with and without PRL.
  • Utilized co-culture systems to evaluate the suppressive capacity of Treg cells in the presence of PRL.

Main Results:

  • Treg cells constitutively express the PRL receptor, while Teff cells require stimulation to induce its expression.
  • Prolactin significantly inhibited the suppressive function of Treg cells in vitro, reducing proliferation.
  • PRL treatment promoted a Th1 cytokine profile, increasing the production of TNF and IFNγ.

Conclusions:

  • PRL receptor expression is constitutive in Treg cells but inducible in Teff cells.
  • Prolactin actively inhibits the suppressive function of Treg cells.
  • PRL-induced inhibition of Treg cells may occur via the promotion of Th1 cytokine secretion.