Sex affects immunity

Pennell, Leesa M.; Galligan, Carole L.; Fish, Eleanor N.

doi:10.1016/j.jaut.2011.11.013

Cited by 362 publications

(332 citation statements)

References 154 publications

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“…The existing research has pointed toward a female advantage in immune protection, mainly due to the immunosuppressive effects of progesterone and testosterone and the immunoenhancing effects of estrogens (Bouman et al 2005;Pennell et al 2012;Giefing-Kröll et al 2015). The incidences of many bacterial, viral, parasitic, and fungal infectious diseases (e.g., leptospirosis, brucellosis, rabies, leishmaniasis, pulmonary tuberculosis, hepatitis A, meningococcal and pneumococcal infections, and seasonal influenza) were found to be substantially higher, and some infectious diseases were shown to be more severe in men than in premenopausal women (Giefing-Kröll et al 2015).…”

Section: Effects Of Sex Hormones On the Immune Systemmentioning

confidence: 99%

Sex Differences in Health and Survival

Oksuzyan

Gumà

Doblhammer

2018

A Demographic Perspective on Gender, Family and Health in Europe

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Section: Effects Of Sex Hormones On the Immune Systemmentioning

confidence: 99%

Sex Differences in Health and Survival

Oksuzyan

Gumà

Doblhammer

2018

A Demographic Perspective on Gender, Family and Health in Europe

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“…Similarly, estrogen usage negatively correlated with the presence of TPO antibodies (83). During the menstrual cycle, lower levels of estrogens during menstruation and luteal phase and higher levels of estrogens during the follicular phase lead to a shift from Th1-to Th2-mediated immunity respectively (84). Accordingly, in young women, levels of the Th2 cytokine interleukin 6 (IL6) negatively correlated with progesterone levels during the normal menstrual cycle.…”

Section: European Journal Of Endocrinologymentioning

confidence: 99%

“…IL6 was shown to inhibit the induction of FOXP3 and, consequently, the generation of Tregs (59). Conversely, estrogens were reported to enhance Treg formation (84). Accordingly, the number of Tregs was shown to decrease during the luteal phase and to increase during the late follicular phase (86).…”

Section: European Journal Of Endocrinologymentioning

confidence: 99%

MECHANISMS IN ENDOCRINOLOGY: Thyroid and polycystic ovary syndrome

Gaberšček

Zaletel

Schwetz

et al. 2015

European Journal of Endocrinology

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Thyroid disorders, especially Hashimoto's thyroiditis (HT), and polycystic ovary syndrome (PCOS) are closely associated, based on a number of studies showing a significantly higher prevalence of HT in women with PCOS than in controls. However, the mechanisms of this association are not as clear. Certainly, genetic susceptibility contributes an important part to the development of HT and PCOS. However, a common genetic background has not yet been established. Polymorphisms of the PCOS-related gene for fibrillin 3 (FBN3) could be involved in the pathogenesis of HT and PCOS. Fibrillins influence the activity of transforming growth factor beta (TGFb). Multifunctional TGFb is also a key regulator of immune tolerance by stimulating regulatory T cells (Tregs), which are known to inhibit excessive immune response. With lower TGFb and Treg levels, the autoimmune processes, well known in HT and assumed in PCOS, might develop. In fact, lower levels of TGFb1 were found in HT as well as in PCOS women carrying allele 8 of D19S884 in the FBN3 gene. Additionally, vitamin D deficiency was shown to decrease Tregs. Finally, high estrogen-to-progesterone ratio owing to anovulatory cycles in PCOS women could enhance the immune response. Harmful metabolic and reproductive effects were shown to be more pronounced in women with HT and PCOS when compared with women with HT alone or with controls. In conclusion, HT and PCOS are associated not only with respect to their prevalence, but also with regard to etiology and clinical consequences. However, a possible crosstalk of this association is yet to be elucidated.

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“…In comparison to men, women are two to three times more prone to develop RA, exhibit a more aggressive disease course and display worse responses to treatments with biological agents [22]. The higher prevalence of RA among women may reflect gender differences in the innate and adaptive immune systems [23,24]. The exact mechanisms underlying this sexual dimorphism in the immune response remain obscure; however, sex hormones, environmental factors and microchimerism have been implicated in this phenomenon [25,26].…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms within the human leucocyte antigen-E gene and their associations with susceptibility to rheumatoid arthritis as well as clinical outcome of anti-tumour necrosis factor therapy

Iwaszko

Świerkot

Kolossa³

et al. 2015

Clinical and Experimental Immunology

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Summary Involvement of the non‐classical human leucocyte antigen‐E (HLA‐E) in both innate and acquired immune response suggests its possible role in development of autoimmune pathologies. This study was undertaken to investigate relationships between the HLA‐E gene single nucleotide polymorphisms (SNPs) and a risk of rheumatoid arthritis (RA), as well as to evaluate a potential of these polymorphisms to modulate clinical outcome of anti‐tumour necrosis factor (TNF) treatment in female patients. A total of 223 female patients with RA receiving anti‐TNF biological therapy and 134 female healthy subjects were enrolled into the study. Genotypings for two SNPs within the HLA‐E gene (rs1264457 HLA‐E*01:01/01:03; rs1059510 HLA‐E*01:03:01/01:03:02) were performed using a polymerase chain reaction (PCR) amplification employing LightSNiP assays. Clinical response was evaluated according to the European League Against Rheumatism (EULAR) criteria at 12 and 24 weeks after initiation of the therapy. The frequency of the HLA‐E*01:01/01:01 genotype was decreased significantly in RA patients in comparison to controls (P = 0·031). The presence of the HLA‐E*01:01/01:01 genotype in patients correlated with better EULAR response after 12 weeks of anti‐TNF treatment, while 01:03 allele carriers were generally unresponsive to the treatment (P = 0·014). The HLA‐E*01:03/01:03 genotype was also over‐represented among non‐responding patients in comparison to HLA‐E*01:01/01:01 homozygotes (P = 0·021). With respect to the HLA‐E rs1059510 variation, a better response after 12 weeks was observed more frequently in patients carrying the HLA‐E*01:03:01/01:03:01 genotype than other genotypes (P = 0·009). The results derived from this study imply that HLA‐E polymorphisms may influence RA susceptibility and affect clinical outcome of anti‐TNF therapy in female RA patients.

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Sex affects immunity

Cited by 362 publications

References 154 publications

Sex Differences in Health and Survival

Sex Differences in Health and Survival

MECHANISMS IN ENDOCRINOLOGY: Thyroid and polycystic ovary syndrome

Polymorphisms within the human leucocyte antigen-E gene and their associations with susceptibility to rheumatoid arthritis as well as clinical outcome of anti-tumour necrosis factor therapy

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