A number of epidemiological studies point toward the sexual dimorphism in the outcome of immune inflammatory responses in infectious and noninfectious diseases. Overall, morbidity and mortality rates are lower in women than in men along the life course thanks to their robust immune defense mechanisms. Yet, ...
A number of epidemiological studies point toward the sexual dimorphism in the outcome of immune inflammatory responses in infectious and noninfectious diseases. Overall, morbidity and mortality rates are lower in women than in men along the life course thanks to their robust immune defense mechanisms. Yet, while useful in short-term defense against acute infection, the strong immune inflammatory response in females may ultimately came at a cost of chronic inflammatory diseases such as cystic fibrosis or chronic obstructive pulmonary disease that are more prevalent and more severe in girls than in boys. With the increasing awareness of the importance of sexually dimorphic immune inflammatory diseases and giving the growing need for gender-based therapy, it is critical to understand the basic mechanisms underlyning the contrasting degree of susceptibility observed between males and females. The mechanisms at work are still scarce and likely to involve multifactorial processes including hormonal differences and sex-specific genetic architecture where X-chromosome-linked genes might play a prominent role.
The purpose of this Research Topic is to shed light on the biomarkers and emerging mechanisms regarding sexually dimorphic immune inflammatory responses and as a means to drive development of new perspectives in the field. Being at the crossroads of immunology, microbiology and inflammatory diseases, this multidisciplinary research topic should bring together community of investigators working on different facet of the subject in humans and also in animal models with the aim to enhance our understanding about the dynamic of sexually dimorphic immunity in inflammatory settings and discuss whether conclusions drawn from animal studies could be extrapolated to the human.
Keywords:
Gender dimorphism, Inflammation, X-linked genes
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