Research article

Sexual dimorphism in immune response genes as a function of puberty

Rebecca Lamason¹ , Po Zhao² , Rashmi Rawat¹ , Adrian Davis¹ , John C Hall¹ , Jae Jin Chae³ , Rajeev Agarwal³ , Phillip Cohen⁴ , Antony Rosen¹ , Eric P Hoffman² and Kanneboyina Nagaraju²

¹  Division of Rheumatology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA

²  Research Center for Genetic Medicine, Children's National Medical Center, 111 Michigan Ave, NW, Washington DC, 20010, USA

³  National Institutes of Health, Bethesda, MD, USA

⁴  University of Pennsylvania, Philadelphia, PA, USA

author email corresponding author email

BMC Immunology 2006, 7:2doi:10.1186/1471-2172-7-2

Published:	22 February 2006

Abstract

Background

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.

Results

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.

Conclusion

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.