Effects of exogenous estrogen on uterine leukocyte recruitment

DeLoia, Julie A.; Stewart‐Akers, Ann M.; Brekosky, Jill; Kubik, Carolyn J.

doi:10.1016/s0015-0282(01)03062-x

Cited by 47 publications

(31 citation statements)

References 32 publications

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“…An explanation for the increase in the concentrations of most mediators after ovarian stimulation may be an increased cytokine expression by endometrial stromal and epithelial cells under the influence of high E 2 and P levels. However, it may also be caused by an increased number of uterine natural killer (uNK) cells present in the endometrium under the influence of supraphysiological levels of E (27) and after ovarian stimulation (28). The uNk cells are the most abundant leukocytes in the luteal phase endometrium and they can secrete an array of cytokines (29), such as VEGF-A, IFN-g, TNF-a, MIF, MCP-1, eotaxin, and IP-10 (30,31).…”

Section: Discussionmentioning

confidence: 99%

Ovarian stimulation for in vitro fertilization alters the intrauterine cytokine, chemokine, and growth factor milieu encountered by the embryo

Boomsma

Kavelaars

Eijkemans

et al. 2010

Fertility and Sterility

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Section: Discussionmentioning

confidence: 99%

Ovarian stimulation for in vitro fertilization alters the intrauterine cytokine, chemokine, and growth factor milieu encountered by the embryo

Boomsma

Kavelaars

Eijkemans

et al. 2010

Fertility and Sterility

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“…Increased leukocyte migration into the uterus was seen in women on oral estrogen (51). Transsexual men receiving estrogens and antiandrogens were also reported to have increased T cell CCR1, CCR5, and CXCR3 expression (52).…”

Section: Discussionmentioning

confidence: 99%

Estrogen Regulates CCR Gene Expression and Function in T Lymphocytes

Mo¹,

Chen²,

Grolleau-Julius³

et al. 2005

The Journal of Immunology

107

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Estrogen has been implicated in the observed female bias in autoimmune diseases. However, the mechanisms behind this gender dimorphism are poorly defined. We have previously reported that in vivo T cell trafficking is gender- and estrogen-dependent. Chemokine receptors are critical determinants of T cell homing and immune response. In this study, we show that the female gender is associated with increased CD4+ T cell CCR1-CCR5 gene and protein expression in mice. The increased CCR expression correlates with enhanced in vitro chemotaxis response to MIP-1β (CCL4). In vivo treatment of young oophorectomized and postmenopausal female mice with 17β-estradiol also increased CD4+ T cell CCR expression. Finally, 17β-estradiol enhances tyrosine phosphorylation in T cells stimulated with MIP-1α in a time-dependent manner. Our results indicate an important role of estrogen in determining T cell chemokine response that may help explain the increased susceptibility and severity of autoimmune diseases in females.

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“…Macrophages are found through most of the menstrual cycle with an increase in the early secretory phase and a further increase in the late secretory phase. Sex hormones such as estrogen and progesterone tightly regulate the distribution of macrophages within endometrium [85][86][87][88]. Macrophages selectively accumulate within premenstrual endometrial stroma, coinciding with decrease of estrogen and progesterone levels that are resulted from the structural degradation and functional loss of the corpus luteum of ovary.…”

Section: Macrophagesmentioning

confidence: 99%