title: Sexual dimorphism in immune response genes as a function of puberty.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Rheumatology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD, USA. rlamaso1@jhmi.edu
authors.forename: Rebecca
authors.initials: R
authors.lastname: Lamason
authors.forename: Po
authors.initials: P
authors.lastname: Zhao
authors.forename: Rashmi
authors.initials: R
authors.lastname: Rawat
authors.forename: Adrian
authors.initials: A
authors.lastname: Davis
authors.forename: John C
authors.initials: JC
authors.lastname: Hall
authors.forename: Jae Jin
authors.initials: JJ
authors.lastname: Chae
authors.forename: Rajeev
authors.initials: R
authors.lastname: Agarwal
authors.forename: Phillip
authors.initials: P
authors.lastname: Cohen
authors.forename: Antony
authors.initials: A
authors.lastname: Rosen
authors.forename: Eric P
authors.initials: EP
authors.lastname: Hoffman
authors.forename: Kanneboyina
authors.initials: K
authors.lastname: Nagaraju
mesh_terms: D000818:Animals; D000917:Antibody Formation; D001402:B-Lymphocytes / Q000187:drug effects / Q000276:immunology; D004967:Estrogens / Q000494:pharmacology / Q000502:physiology*; D053222:Fas Ligand Protein; D005260:Female; D020869:Gene Expression Profiling; D018507:Gene Expression Regulation, Developmental / Q000187:drug effects; D005802:Genes, MHC Class II; D006242:Haptoglobins / Q000032:analysis; D007371:Interferon-gamma / Q000032:analysis; D008213:Lymphocyte Activation; D008297:Male; D008562:Membrane Glycoproteins / Q000235:genetics / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D019463:Mice, Inbred MRL lpr; D008817:Mice, Mutant Strains / Q000235:genetics; D000685:Serum Amyloid A Protein / Q000032:analysis; D012727:Sex Characteristics; D012741:Sexual Maturation / Q000276:immunology*; D013154:Spleen / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000187:drug effects / Q000276:immunology; D048069:Tumor Necrosis Factors / Q000235:genetics / Q000502:physiology; D019014:fas Receptor / Q000235:genetics / Q000502:physiology
chemical_list: D004967:Estrogens; D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D006242:Haptoglobins; D008562:Membrane Glycoproteins; D000685:Serum Amyloid A Protein; D048069:Tumor Necrosis Factors; D019014:fas Receptor; D007371:Interferon-gamma