Background: It has been suggested that estrogen may enhance humoral immune
responses and may be involved in the pathogenesis of autoimmune diseases,
Objective: We studied the in vitro effects of 17 beta-estradiol (E-2) on sp
ontaneous immunoglobulin production by human PBMCs.
Methods: PBMCs from healthy human volunteers were cultured with E-2. Levels
of IgG and IgM and cytokine activity were measured by ELISA, proliferation
was determined by [H-3]-thymidine uptake. The cell viability was assessed
by a trypan blue exclusion test.
Results: E-2 enhanced IgG and IgM production of PBMCs both from men and wom
en without altering cell viability and proliferation, The stimulatory effec
t of E-2 was revealed at 10(-10) mol/L, increased in a dose-dependent fashi
on, and was maximized at 10(-8) mol/L, IgG production of PBMCs in the prese
nce of E-2 (10(-8) mol/L) was 220% of control cells, and that of IgM was 21
1%. Immunoglobutin production of E-2-treated B cells was slightly higher th
an that of control cells; IgG production was 161% of control cells, and tha
t of IgM was 157%. Anti-IL-10 antibody partially blocked the E-2 effect on
immunoglobulin production of PBMCs; anti-IL-10 reduced IgG production in th
e presence of E-2 from 206% to 151% of control cells, and that of IgM from
206% to 152%. E-2 increased IL-10 production of monocytes up to 250% of con
trol level, but it did not affect that of T cells or B cells. Exogenous IL-
10 (1 U/mL) further enhanced E-2-induced increase of immunoglobulin product
ion by B cells, although this level of IL-10 alone was ineffective for B ce
lls.
Conclusion: These results suggest that E2 may increase immunoglobulin produ
ction of human PBMCs mainly by increasing IL-10 production of monocytes, Th
e results also support that E-2 may act as an important stimulator for huma
n humoral immunity.