Females are more resistant to certain infections, and suffer a higher incidence of autoimmune diseases. Immune disease expression is also affected by the reproductive status of the female. Indeed, the decline in ovarian function with menopause is associated with spontaneous increase in pro-inflammatory cytokines, tumor necrosis factor-α (TNF-α), interleukin-1 and interleukin-6. In general, estradiol seems to have anti-inflammatory effects on neutrophils, while progesterone seems to have pro-inflammatory effects on these cells. In males an increase in blood monocyte number is demonstrated as compared to females during menopause in the follicular phase. Increased potency to lyse other cells is found in postmenopausal females and in males as compared to females with a regular menstrual cycle. This is in line with the fact that natural killer (NK) cell activity is also decreased in postmenopausal females using hormone replacement therapy. In vitro estrogens appear to suppress NK cell activity. Estrogens appear to increase the numbers and function of regulatory T lymphocytes, which inhibit the adaptive immune response. In contrast, progesterone may counteract the estrogen effects. Sex differences in immune responses therefore account for, at least in part, the sex differences in incidence and progression of liver disease.
Keywords: TNF-αa, interleukin-1, interleukin-6, estradiol, progesterone, testosterone, menopause, hormone replacement therapy, cytotoxic T cell, NK cell, regulatory T cell, immune system
