Sex Hormones and Immune Responses

1999 ◽  
pp. 163-181 ◽  
Author(s):  
William J. Kovacs ◽  
Nancy J. Olsen
Keyword(s):  
Immune Responses ◽  
Sex Hormones

scholarly journals Microbiome, sex hormones, and immune responses in the reproductive tract: Challenges for vaccine development against sexually transmitted infections

Vaccine ◽  
2014 ◽  
Vol 32 (14) ◽  
pp. 1543-1552 ◽  
Author(s):  
Rebecca M. Brotman ◽  
Jacques Ravel ◽  
Patrik M. Bavoil ◽  
Patti E. Gravitt ◽  
Khalil G. Ghanem
Keyword(s):  
Immune Responses ◽  
Sexually Transmitted Infections ◽  
Sex Hormones ◽  
Reproductive Tract ◽  
Vaccine Development ◽  
Sexually Transmitted

scholarly journals An overview of sex hormones in relation to SARS-CoV-2 infection

2021 ◽  
Author(s):  
Marzieh Saei Ghare Naz ◽  
Mojdeh Banaei ◽  
Sareh Dashti ◽  
Fahimeh Ramezani Tehrani
Keyword(s):  
Sex Differences ◽  
Immune System ◽  
Literature Review ◽  
Immune Responses ◽  
Sex Hormones ◽  
Web Of Science ◽  
Vaccine Development ◽  
Response To Treatment ◽  
Different Seasons ◽  
Body Response

Aim: Sex differences in COVID-19 outcomes might be explained from a sex hormones (SexHs) perspective. Materials & methods: PubMed, Scopus, Web of Science, EMBASE and Google Scholar were searched up to March 2021. Results: Based on the literature review, the crosstalk between SexHs (estrogens, progesterone and testosterone), their receptors (estrogen α and β, androgen, and progesterone) and the immune system shaped the sex-related differences in immune responses against COVID-19. Differential production of SexHs over the lifespan (during pregnancy, reproductive years, menopause and andropause) and over different seasons may result in disparities in body response toward COVID-19. Moreover, SexHs-specific differences might affect vaccine efficacy and response to treatment. Conclusion: The roles of SexHs need to be considered in vaccine development and even treatment of COVID-19.

scholarly journals 17β-Estradiol Dysregulates Innate Immune Responses to Pseudomonas aeruginosa Respiratory Infection and Is Modulated by Estrogen Receptor Antagonism

2017 ◽  
Vol 85 (10) ◽  
Author(s):  
Shadaan Abid ◽  
ShangKui Xie ◽  
Moumita Bose ◽  
Philip W. Shaul ◽  
Lance S. Terada ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Estrogen Receptor ◽  
Immune Responses ◽  
Sex Hormones ◽  
Inflammatory Responses ◽  
Human Subjects ◽  
Content Type ◽  
Female Mice ◽  
17Β Estradiol ◽  
The Impact

ABSTRACT Females have a more severe clinical course than males in terms of several inflammatory lung conditions. Notably, females with cystic fibrosis (CF) suffer worse outcomes, particularly in the setting of Pseudomonas aeruginosa infection. Sex hormones have been implicated in experimental and clinical studies; however, immune mechanisms responsible for this sex-based disparity are unknown and the specific sex hormone target for therapeutic manipulation has not been identified. The objective of this study was to assess mechanisms behind the impact of female sex hormones on host immune responses to P. aeruginosa. We used wild-type and CF mice, which we hormone manipulated, inoculated with P. aeruginosa, and then examined for outcomes and inflammatory responses. Neutrophils isolated from mice and human subjects were tested for responses to P. aeruginosa. We found that female mice inoculated with P. aeruginosa died earlier and showed slower bacterial clearance than males (P < 0.0001). Ovariectomized females supplemented with 17β-estradiol succumbed to P. aeruginosa challenge earlier than progesterone- or vehicle-supplemented mice (P = 0.0003). 17β-Estradiol-treated ovariectomized female mice demonstrated increased lung levels of inflammatory cytokines, and when rendered neutropenic the mortality difference was abrogated. Neutrophils treated with 17β-estradiol demonstrated an enhanced oxidative burst but decreased P. aeruginosa killing and earlier cell necrosis. The estrogen receptor (ER) antagonist ICI 182,780 improved survival in female mice infected with P. aeruginosa and restored neutrophil function. We concluded that ER antagonism rescues estrogen-mediated neutrophil dysfunction and improves survival in response to P. aeruginosa. ER-mediated processes may explain the sex-based mortality gap in CF and other inflammatory lung illnesses, and the ER blockade represents a rational therapeutic strategy.

scholarly journals Rheumatoid Arthritis: A Female Challenge

2008 ◽  
Vol 4 (2) ◽  
pp. 195-201 ◽  
Author(s):  
M Gerosa ◽  
V De Angelis ◽  
P Riboldi ◽  
PL Meroni
Keyword(s):  
Rheumatoid Arthritis ◽  
Immune Responses ◽  
Sex Hormones ◽  
Antiphospholipid Antibodies ◽  
Strong Association ◽  
Hormonal Treatment ◽  
Antirheumatic Drugs ◽  
Hormonal Profile ◽  
Patients Experience ◽  
Common Situation

Rheumatoid arthritis (RA) is two- to three-fold more frequent in women than in men and a strong association with sex hormones has been demonstrated. There is strong evidence that autoimmunity is under genetic control, and genes in sexual chromosomes can play a role in supporting the female prevalence. On the other hand, it is widely accepted that sex hormones – estrogens in particular – may regulate the immune response by favoring the survival of forbidden autoreactive clones and ultimately the prevalence of autoimmunity in women. Accordingly, estrogens have been suggested to be associated with the development of RA. Pregnancy in RA women is a common situation and most pregnant patients experience a remission. This has been closely related to a switch from Th1 to Th2 immune responses and to a decreased production of proinflammatory cytokines, at least in part supported by the changes of the hormonal profile in pregnancy. Pregnancy planning is required in RA in order to avoid unwanted complications. In particular, the need to control the disease requires safe use of antirheumatic drugs both during the pregnancy itself and in the breastfeeding period. Hormonal treatment for contraception is contraindicated in the case of positivity for antiphospholipid antibodies owing to the increased thrombophilic risk. Similarly, replacement hormonal treatment in postmenopausal women with RA to control osteoporosis is no longer recommended as a result of its ability to increase the cardiovascular risk closely associated with RA itself.

scholarly journals Sex-Dependent Outcome of Hepatitis B and C Viruses Infections: Synergy of Sex Hormones and Immune Responses?

2018 ◽  
Vol 9 ◽  
Author(s):  
Anna Ruggieri ◽  
Maria Cristina Gagliardi ◽  
Simona Anticoli
Keyword(s):  
Hepatitis B ◽  
Immune Responses ◽  
Sex Hormones

scholarly journals GENDER DIFFERENCES AND THE EFFECTS OF SEX HORMONES ON IMMUNE RESPONSES FOLLOWING HEMORRHAGE AND SEPSIS.

Shock ◽  
1997 ◽  
Vol 7 (Supplement) ◽  
pp. 100
Author(s):  
I H Chaudry ◽  
M W Wichmann ◽  
R Zellweger ◽  
M Angele ◽  
A Ayala
Keyword(s):  
Gender Differences ◽  
Immune Responses ◽  
Sex Hormones

scholarly journals Sex hormones, autoimmune diseases, and immune responses.

BMJ ◽  
1991 ◽  
Vol 303 (6793) ◽  
pp. 2-3 ◽  
Author(s):  
A M Denman
Keyword(s):  
Immune Responses ◽  
Autoimmune Diseases ◽  
Sex Hormones

scholarly journals The Roles of Sex Hormones in the Course of Atopic Dermatitis

2019 ◽  
Vol 20 (19) ◽  
pp. 4660 ◽  
Author(s):  
Kanda ◽  
Hoashi ◽  
Saeki
Keyword(s):  
Atopic Dermatitis ◽  
Immune Responses ◽  
Sex Hormones ◽  
Sexual Difference ◽  
Skin Barrier ◽  
Dehydroepiandrosterone Sulfate ◽  
Skin Permeability ◽  
Permeability Barrier ◽  
Nickel Allergy ◽  
T Helper 2

Atopic dermatitis (AD) is a chronic inflammatory skin disease characterized by T helper 2 cell (Th2)-shifted abnormal immunity, skin barrier impairment, and pruritus. The prevalence of AD in childhood is slightly higher in boys than in girls; after puberty, the sexual difference is reversed. The female preponderance in all generations exists in intrinsic AD with enhanced Th1 activity and nickel allergy, lacking increased serum IgE or filaggrin mutation. AD is often deteriorated before menstruation. We review the effects of sex hormones on immune responses and skin permeability barrier and propose possible hypotheses for the above phenomena. After puberty, the immune responses of patients are remarkably influenced by sex hormones. Estrogen and progesterone enhance the activities of Th2/regulatory T cell (Treg) but suppress Th1/Th17. Androgens suppress Th1/Th2/Th17 and induce Treg. The skin permeability barrier is fortified by estrogen but is impaired by progesterone and androgens. Dehydroepiandrosterone suppresses Th2 but enhances Th1. The amount of steroid sulfatase converting dehydroepiandrosterone sulfate to dehydroepiandrosterone is higher in women than in men, and thus, women might be more susceptible to the influence of dehydroepiandrosterone. The balance of modulatory effects of sex hormones on immune responses and skin barrier might regulate the course of AD.

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