Abstract
Sexual dimorphism in the mammalian immune system is manifested as more frequent and severe infectious diseases in males and, on the other hand, higher rates of autoimmune disease in females, yet insights underlying those differences are still lacking. Here we characterize sex differences in the immune system by RNA and ATAC sequence profiling of untreated and interferon-induced immune cell types in male and female mice. We detect very few differentially expressed genes between male and female immune cells except in macrophages from three different tissues. Accordingly, very few genomic regions display differences in accessibility between sexes. Transcriptional sexual dimorphism in macrophages is mediated by genes of innate immune pathways, and increases after interferon stimulation. Thus, the stronger immune response of females may be due to more activated innate immune pathways prior to pathogen invasion.
Highlights
Sexual dimorphism in the mammalian immune system is manifested as more frequent and severe infectious diseases in males and, on the other hand, higher rates of autoimmune disease in females, yet insights underlying those differences are still lacking
Sexual dimorphism of the immune system is not limited to mammals but extends to birds, where the heterogametic sex is female, but still mortality rates from infectious diseases are higher in males[12]
To assess whether the identified transcriptional sexual dimorphism is relevant to the phenotypic sexual dimorphism, we focused on the most sex-biased autoimmune disease, systemic lupus erythematosus (SLE)
Summary
Sexual dimorphism in the mammalian immune system is manifested as more frequent and severe infectious diseases in males and, on the other hand, higher rates of autoimmune disease in females, yet insights underlying those differences are still lacking. It is possible that systemic or tissue-specific X inactivation or escape from inactivation, together with X- and Y-linked immune-related genes, cause immunological differences between males and females[14]. The X-linked gene Tlr[7] plays a role in innate immune response and displays higher expression in females compared to males, potentially due to incomplete X-inactivation[16]. Another example of this potential effect is the. Pregnancy depresses maternal immunity as a means of preventing rejection of the fetus[19]
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