Sexual dimorphism in immune response genes as a function of puberty

BMC Immunology
Rebecca LamasonKanneboyina Nagaraju

Abstract

Autoimmune diseases are more prevalent in females than in males, whereas males have higher mortality associated with infectious diseases. To increase our understanding of this sexual dimorphism in the immune system, we sought to identify and characterize inherent differences in immune response programs in the spleens of male and female mice before, during and after puberty. After the onset of puberty, female mice showed a higher expression of adaptive immune response genes, while males had a higher expression of innate immune genes. This result suggested a requirement for sex hormones. Using in vivo and in vitro assays in normal and mutant mouse strains, we found that reverse signaling through FasL was directly influenced by estrogen, with downstream consequences of increased CD8+ T cell-derived B cell help (via cytokines) and enhanced immunoglobulin production. These results demonstrate that sexual dimorphism in innate and adaptive immune genes is dependent on puberty. This study also revealed that estrogen influences immunoglobulin levels in post-pubertal female mice via the Fas-FasL pathway.

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Methods Mentioned

BETA
ELISA
flow cytometry
in vitro transcription
chips
enzyme-linked immunosorbent assay
ELISAs

Software Mentioned

Cell Quest
Public Expression Profiling Resource
Affymetrix Microarray Laboratory Information Management System...
Microarray Suite

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