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Modulation of Maternal LIF Producers T Cells by Trophoblast and Paternal Antigens
Author(s) -
Fraccaroli Laura,
Grasso Esteban,
Zeitler Elena,
Lombardi Eduardo,
Gogorza Sebastián,
Etchepareborda Juan José,
Nagle Carlos,
Cortelezzi Marta,
Leirós Claudia Pérez,
Ramhorst Rosanna
Publication year - 2011
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.2010.00890.x
Subject(s) - trophoblast , leukemia inhibitory factor , antigen , vasoactive intestinal peptide , endocrinology , medicine , andrology , fetus , cell culture , biology , pregnancy , chemistry , placenta , immunology , receptor , interleukin 6 , inflammation , neuropeptide , genetics
Citation Fraccaroli L, Grasso E, Zeitler E, Lombardi E, Gogorza S, Etchepareborda JJ, Nagle C, Cortelezzi M, Leirós CP, Ramhorst R. Modulation of maternal LIF producers T cells by trophoblast and paternal antigens. Am J Reprod Immunol 2011; 65: 133–145 Problem Fetal implantation enhances the production of essential growth factors such as LIF (leukaemia inhibitory factor), hence we investigated the contribution of maternal CD4 cells, activated by paternal or trophoblast antigens and its modulation by VIP (vasoactive intestinal peptide) and progesterone. Method of study We performed co cultures of trophoblast cells (Swan‐71 cell line) or paternal antigens and PBMCs from patients with recurrent spontaneous abortions (RSA) and fertile women. Result Fertile‐CD4 + LIF + cells were increased by VIP and progesterone in response to paternal and trophoblast antigens. Also MMP‐9 activity was decreased and pSTAT3/STAT3 ratio was increased. RSA patients have decreased levels of LIF expression which could not be modulated by VIP and progesterone and displayed a reduced number of endometrial infiltrated CD4 + LIF + cells compared with fertile women. Conclusion The decrease of CD4 + LIF + cells in RSA patients could be related with the exacerbated inflammatory response observed in the maternal‐fetal dialogue model.