Genetic risk alleles that interact with estrogenic factors underlie women’s RA susceptibility.
Infectious agents and smoking add complexity to this gene-estrogen interaction.
The biological mechanisms leading to RA may differ between pre- and post-menopausal women.
Postmenopausal RA is hypothesized to be characterized by seropositivity for ACPA.
Postmenopausal ACPA(+) RA results of skewed CD4+ T cell profile and derived cytokines.