Regulatory mechanisms of IL-13 signaling pathway/role in normal gestation

crossMark
doi: 10.18081/2333-5106/015-08/468-480
Received November 04, 2017; Accepted March 11, 2018; Published April 13, 2018

Marchil Carden, Maria Granger, Marchil G. Rovere, Amanda Bron, Jimmy Fukumoto

Abstract

In the gestational process, the immune response is regulated by a complex network of cytokines secreted by Th1 and Th2 T helper lymphocytes, acting antagonistically. The most important cytokines with a predominant Th2 profile are those controlling specific isotype reactivity (IL-4) and production of secretory IgA (sIgA), which protects the mucous membrane of the uterus against bacterial infections during pregnancy, and atrophy of the tissue due to estrogen accumulation (IL-10) after Th1 response occurring during childbirth. A specific anti-inflammatory cytokine controlling both cytokine-producing earlier, IL-4 and INF-g, is represented by IL-13. It has been demonstrated that IL-13 is also endowed with strong biological activities in indications such as asthma and anaplasmosis since its numerous bioactivities can be regulated to a great extent by the multi-functional IL-13R. In summary, IL-13 is a cytokine involved in processes such as immunoglobulin IgE production, IgA switching, mucus secretion, peripheral blood mononuclear cells apoptosis, etc., and in cases of pregnancy, it is expected to influence Th1-type responses. It is mainly proposed not only to neutralize infectious agents transported locally to the uterus but also responsible, among others, for the potent antiphlogistic effect: IL-13 suppresses IL-4 and IFN-g production from Th1 and/or Th2 lymphocyte cells simultaneously. The difference in signaling pathways, transduction, target tissues, and cellular response, through the specificity of functional IL-13R, and those that are expressed in the major cellular targets, maternal decidual cell vs trophoblast cells, may explain the various actions of the progestational factor in the deciduo-trophoblast interface homeostasis.

Keywords: IL-13; Nnormal pregnancy; Fetal development; IL-4

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