Mini puberty and its interpretation

Kurtoğlu, Selim; Baştuğ, Osman

doi:10.5152/tpa.2014.2038

Cited by 53 publications

(57 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…After birth, hormonal levels peak shortly due to the activation of the hypothalamo‐pituitary‐gonadal axis, during the so‐called “mini puberty.” In this period, sex hormone levels are comparable to the period of early‐middle puberty . Estrogens are able to interact with the immune system by binding to estrogen receptors (ERs) on different immune cells, including monocytes .…”

Section: Introductionmentioning

confidence: 97%

The impact of sex hormones on BCG-induced trained immunity

Bree

Janssen

Aaby

et al. 2018

Journal of Leukocyte Biology

View full text Add to dashboard Cite

The anti-tuberculosis vaccine Bacillus Calmette-Guérin (BCG) is a well-known immune modulator that induces nonspecific protective effects against heterologous infections through induction of innate immune memory, also termed "trained immunity." In randomized trials in low weight newborns, BCG vaccination reduced neonatal mortality due to decreased incidence of sepsis and respiratory infections. In many studies, sex-differential nonspecific effects of vaccines have been observed, but the mechanisms behind these differential effects are unknown. We investigated whether the important sex hormones estrogen and dihydrotestosterone (DHT) influence BCG-induced trained immunity in human primary monocytes. Although addition of estradiol and DHT to BCG inhibited the production of proinflammatory cytokines after direct stimulation of human monocytes, they did not influence the induction of trained immunity by BCG. In addition, estradiol or DHT did not induce training or tolerance in monocytes themselves. We conclude that these important sex hormones are unlikely to explain the sex-differential effects after BCG vaccination. Future studies should focus on the investigation of alternative mechanisms as an explanation for sex-differential nonspecific effects of BCG vaccination.

show abstract

Section: Introductionmentioning

confidence: 97%

The impact of sex hormones on BCG-induced trained immunity

Bree

Janssen

Aaby

et al. 2018

Journal of Leukocyte Biology

View full text Add to dashboard Cite

show abstract

“…Do sex hormones also influence FEZF2 expression? Third, sex hormone profiles are not only different between males and females after puberty, but also in the first six months of life, when neonates undergo "mini-puberty" with adult levels of circulating sex hormones (20). Are differences in AIRE expression already present at this early time period?…”

mentioning

confidence: 99%

Estrogen turns down “the AIRE”

Bakhru¹,

Su²

2016

Journal of Clinical Investigation

View full text Add to dashboard Cite

C o m m e n t a r yAutoimmune disease: sex-dependent differencesThe incidence of autoimmune disease is increasing worldwide; therefore, the need to understand the basis of autoimmunity has taken on a new urgency. Progress in identifying genetic contributors to autoimmunity has been made through the study of monogenic autoimmune diseases. Such an approach has identified critical immuneregulatory genes, such as the autoimmune regulator (AIRE), which encodes a nuclear protein that functions as a key regulator of thymic central tolerance (reviewed in ref. 1). AIRE enforces self tolerance by promoting the promiscuous expression of tissue self-antigens (TSAs) within medullary thymic epithelial cells (mTECs), a nonhematopoietic, stromal cell population (Figure 1A). Presentation of these TSAs within the thymus results in negative selection of bone marrow-derived T cells, which recognize these TSAs with high affinity. In addition to eliminating autoreactive T cell clones within the thymus, AIRE also maintains self tolerance by diverting autoreactive T cells into the Treg lineage. AIRE is important for preventing autoimmune disease, as individuals with a complete loss of AIRE function develop the multiorgan autoimmune disease autoimmune polyendocrinopathy syndrome type 1 (APS1, which is also known as autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy [APECED]). While genetics are a major factor that determines autoimmune disease predisposition, it is clear that sex also plays a defining role in disease development. The incidence of autoimmunity is skewed toward females for many autoimmune diseases, including Sjögren's disease, systemic lupus erythematosus (SLE), and autoimmune thyroid disease (reviewed in ref. 2). Remarkably, over 80% of those affected with these conditions are female, illustrating the strong influence of sex in disease predisposition. Multiple factors likely underlie this sex bias, including the distinct sex hormone profiles in females versus males. Accumulating evidence suggests that male androgen hormones are immune suppressive, while female estrogen hormones are immune activating. For instance, androgen increases the differentiation of immunoregulatory CD4+ T cells (3), whereas estrogen enhances survival of T cells in patients with autoimmunity (4). Thus, there is a plethora of evidence that sex hormones directly modulate T cells in the periphery.Early clues that sex hormones may also modulate thymic stromal populations, such as mTECs, came from elegant studies that utilized bone marrow chimeras (5, 6). These studies showed that thymic epithelial cells express estrogen receptor (ER) and androgen receptor (AR) and that expression of these hormone receptors in the stromal compartment is required for altering bone marrow-derived T cell subsets in the thymus (5, 6). In this issue, Dragin et al. confirm that sex hormones indeed act on receptors on thymic stromal cells to impinge upon T cell development within the thymus. Furthermore, this study demonstrates that sex hormones regulate AIRE expre...

show abstract

“…Minipuberty is a normal finding as a result of gonadotropin inhibition discontinuing with placental separation; the HPG axis is activated and mildly elevated oestradiol with high FSH levels are noted in early months 5 6. Oedema is thought to be a result of excessive stimulation of LH/hCG receptors resulting in higher concentrations of LH or hCG together with stimulation of FSH receptors,5 but the precise pathophysiology remains greatly unknown.…”

Section: Discussionmentioning

confidence: 99%

Atypical case of preterm ovarian hyperstimulation syndrome

2017

View full text Add to dashboard Cite

Preterm ovarian hyperstimulation syndrome is a rare syndrome in which preterm infant girls have hypogastric, upper leg and labial swelling accompanied by elevated serum oestradiol levels and ovarian follicular cysts on ultrasound. Our case is an infant born at 23 weeks gestational age who at 30 weeks postconceptional age (PCA) developed elevated 17-hydroxyprogesterone on her newborn screen with associated clitoromegaly and a ventral groove on the inferior aspect of the erectile tissue. An initial pelvic ultrasound at 32 weeks PCA demonstrated a normal appearing uterus, but the ovaries were not visualised. At 39 weeks PCA, follicular ovarian cysts were noted bilaterally (31×26×21 mm on left and 38×25×36 mm on right). Without treatment, oestradiol and testosterone levels began normalising by 42 weeks PCA. After this point, the right ovarian cysts had resolved and the left ovarian cyst continued to diminish in size.

show abstract

Mini puberty and its interpretation

Cited by 53 publications

References 47 publications

The impact of sex hormones on BCG-induced trained immunity

The impact of sex hormones on BCG-induced trained immunity

Estrogen turns down “the AIRE”

Atypical case of preterm ovarian hyperstimulation syndrome

Contact Info

Product

Resources

About