Sex differences in immune responses to infectious diseases

Fischer, Julia; Jung, Norma; Robinson, Nirmal; Lehmann, Clara

doi:10.1007/s15010-015-0791-9

Cited by 150 publications

(145 citation statements)

References 47 publications

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“…The onset of puberty is associated with the numbers and functions of circulating granulocytes and monocytes, which are decreased but activated in females due to rising levels of progesterone in the setting of ovulation or pregnancy (7, 8). In addition, myeloid cells and lymphocytes express receptors for estrogen, progesterone and androgens, which orchestrate transcriptional pathways, ligand dependent or ligand independent signaling cascades that influence innate and adaptive immune responses to viruses (9–12). With regard to gene dosage on sex chromosomes, X-linked genes such as IL-13, IL-4, IL-10, Xist, Tlr7, FoxP3 on X chromosome and Sry (testis-determining factor), Sox9 (SRY-box 9) on Y chromosome may underlie sexually dimorphic responses that contribute to stronger innate, cellular and humoral immune responses and susceptibility to autoimmune diseases in females compared with males (13–15).…”

Section: Introductionmentioning

confidence: 99%

Sex Drives Dimorphic Immune Responses to Viral Infections

Ghosh

Klein

2017

The Journal of Immunology

199

158

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New attention to sexual dimorphism in normal mammalian physiology and disease has uncovered a previously unappreciated breadth of mechanisms by which females and males differentially exhibit quantitative phenotypes. Thus, in addition to the established modifying effects of hormones, which prenatally and post-pubertally pattern cells and tissues in a sexually dimorphic fashion, sex differences are caused by extra-gonadal and dosage effects of genes encoded on sex chromosomes. Sex differences in immune responses, especially during autoimmunity, have been studied predominantly within the context of sex hormone effects. More recently, immune response genes have been localized to sex chromosomes themselves or found to be regulated by sex chromosome genes. Thus, understanding how sex impacts immunity requires the elucidation of complex interactions between sex hormones, sex chromosomes and immune response genes. In this brief review, we discuss current knowledge and new insights into these intricate relationships in the context of viral infections.

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Section: Introductionmentioning

confidence: 99%

Sex Drives Dimorphic Immune Responses to Viral Infections

Ghosh

Klein

2017

The Journal of Immunology

199

158

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“…Previous studies have shown that girls produce stronger immune responses to several viruses [12,13]. Thus, our observation may reflect a difference in immune responsiveness to influenza A virus rather than in the number of infections per se.…”

Section: Discussionmentioning

confidence: 56%

Influenza A virus antibodies show no association with pancreatic islet autoantibodies in children genetically predisposed to type 1 diabetes

et al. 2015

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Aims/hypothesis Viral infections have long been considered potential triggers of beta cell autoimmunity and type 1 diabetes. Recent studies have suggested that influenza A virus might increase the risk of type 1 diabetes. The present study evaluates this risk association in prospectively observed children at the time when islet autoimmunity starts and autoantibodies are first detected. Methods IgG class antibodies to influenza A virus were analysed in 95 case children whose antibody screening test turned permanently positive for two or more islet autoantibodies and from 186 autoantibody-negative and non-diabetic control children who were matched for time of birth, sex, date of sampling and HLA-conferred risk of diabetes in the Finnish Type 1 Diabetes Prediction and Prevention (DIPP) study. Virus antibodies were measured from the first autoantibody-positive sample using an enzyme immunoassay. None of the children had been vaccinated against influenza A. Results The prevalence of influenza A virus antibodies did not differ between the case and control children (42% vs 38%; p=0.392) and the median antibody levels were also comparable in the two groups (3.0 vs 3.8 enzyme immunoassay units). A similar result was obtained when case and control children were compared separately in subgroups according to different sex, age and HLA-DQ genotype. However, girls had higher antibody levels than boys among both case and control children (median antibody levels 9.0 vs 2.3 enzyme immunoassay units; p=0.01). Conclusions/interpretation Our results suggest that influenza A infections are not associated with the development of islet autoimmunity in young children with increased genetic susceptibility to type 1 diabetes.

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“…It is widely recognised that females exhibit more robust innate and adaptive immune responses to self and foreign antigens than males, which is thought to be due to hormonal, genetic and environmental influences . Inflammation appears to be a common underlying feature of many disorders that disproportionally affect women and glucocorticoids are a cornerstone in the treatment of many inflammatory disorders .…”

Section: Discussionmentioning

confidence: 99%

Sex‐based differences in the response to dexamethasone in bacterial meningitis: Analysis of the European dexamethasone in adulthood bacterial meningitis study

Dias

Brouwer

Beek

2020

Brit J Clinical Pharma

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Inflammatory markers have been found at higher concentrations in women than men with bacterial meningitis. To investigate sex‐based differences in the response to dexamethasone, we performed a post hoc analysis of a double‐blind, randomised multicentre trial of dexamethasone (10 mg, 4 times daily for 4 days) vs placebo in adults with bacterial meningitis. The primary outcome measure was the Glasgow outcome scale score at 8 weeks and interaction tests were used to examine subgroup differences. Between June 1993 and December 2001, 301 patients (56% male) were randomly assigned to a treatment group: 157 received dexamethasone and 144 placebo. Although dexamethasone reduced the risk of unfavourable outcome to a greater extent in women (relative risk [RR] 0.42, 95% confidence interval [CI] 0.21–0.86, P = .02) than men (RR 0.79, 95% CI 0.41–1.51, P = .55), on interaction testing (ratio of RR women:men 0.53, 95% CI 0.20–1.39, P = .19) patient sex was not a significant modifier of the effect of dexamethasone.

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Sex differences in immune responses to infectious diseases

Abstract: Understanding sex-based differences in immunity during different infectious diseases is crucial in order to provide optimal disease management for both sexes.

Cited by 150 publications

References 47 publications

Sex Drives Dimorphic Immune Responses to Viral Infections

Sex Drives Dimorphic Immune Responses to Viral Infections

Influenza A virus antibodies show no association with pancreatic islet autoantibodies in children genetically predisposed to type 1 diabetes

Sex‐based differences in the response to dexamethasone in bacterial meningitis: Analysis of the European dexamethasone in adulthood bacterial meningitis study

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