IL33 |
IL33 regulates the factors essential for decidual receptivity
during the implantation window. |
[119] |
IL11 |
It is a vital cytokine associate with decidualization,
implantation as well as placentation. |
[119,
165-167] |
dNK cells |
They primarily support the trophoblasts incursion and
vascular modification to facilitate the maximization of the process of
placental perfusion which is possibly under the control of cytokine and
chemokines expression. |
[229, 230] |
IFNγ |
It causes the activation of macrophages present in decidua which
in turn manufacture the factors such as NO and TNFα that may well cause
pregnancy loss. |
[234-236] |
IL4 and IL10 |
They could impede the functions both of Th1 type of cells
as well as macrophages that prevent the feto-allograft dismissal. |
[234-236] |
IFNγ, IL4, IL6, TNFα, TGFβ, M-CSF and LIF receptors |
These receptors
existing on the surface of trophoblastic cells could mediate the effect
of cytokines produced by T cells directly on the growth and role of
trophoblasts. |
[234-236] |
M-CSF (macrophage colony stimulating factor) |
This factor is
responsible for inciting trophoblast proliferation in addition of the
formation of syncytium from cytotrophoblast via differentiation process. |
[237, 238] |
LIF(Leukemia-inhibitory factor) |
Essential for endometrial implantation
and fetal development. |
[239] |
IL8 |
One of the pro-angiogenic cytokines responsible for stimulating
endothelial cell proliferation and capillary tube formation. |
[309] |
IL10 |
Expressed at materno-embryonic interface and inhibits the
formation and role of proinflammatory cytokines such as IL1, IL12, IFNγ
etc. It also stimulates the tolerogenic dendritic cell production |
[24, 241-243, 245] |
IL15 |
This interleukin is considered as a key factor for stimulating
in-vivo proliferation of uNK cells. |
[183] |
TNFα and IFNγ |
They hamper the development of embryo and the production
of trophoblasts lineages in human due to their cytotoxic effect on the
embryonic fibroblast like cells. |
[255, 256] |
TNFα |
During pregnancy it along with hormones brings about thrombosis
in placental tissue and shows increased synthesis at the time of onset
of labor and miscarriage. |
[286] |
|
TNFα has been found linked with the process of inflammation associated
with implantation, placentation, and pregnancy outcome. |
[224] |
Foxp3 Mrna |
Diminished expression in endometrial tissue is linked with
primary idiopathic infertility. |
[300] |
|
The trophoblasts of RPL patients show decreased expression of Foxp3 |
[301] |
Treg cells |
They down regulate the inflammatory responses and protects
the developing embryo. Further, they impede the cytokine synthesis in
CD4+ and CD8+ T cells, cytotoxicity of Natural killer cells and
dendritic cell maturation and function as a result of which the
activation of local inflammation is suppressed. In absence of the Treg
cell mediated modulation there is the possibility of collapse of
pregnancy. |
[9, 302-304] |
|
Decreased percentage of decidual Treg cells has been associated with
miscarriage pathogenesis. |
[310] |
|
The materno-embryonic tolerance mediated by Treg cells has been
reported critical for the establishment allogenic pregnancy. |
[310] |
Micro-RNA (miR-155) |
The reduced level of immune-regulatory microRNA
miR-155 has been observed in RPL which suggests the role of miR-155 in
immune tolerance during pregnancy. miR-155 is a vital regulator of
immune adaptation to pregnancy and is essential for adequate Treg cell
to attain strong pregnancy tolerance and protect against embryonic loss. |
[311] |
Endometrial EGR1 |
The decreased levels of EGR1 have been observed in
women that experience recurrent implantation failure. |
[10] |