RESEARCH SUPPORT, NON-U.S. GOV'T
Estrogen enhances immunoglobulin production by human PBMCs.
Journal of Allergy and Clinical Immunology 1999 Februrary
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 17beta-estradiol (E2 ) on spontaneous immunoglobulin production by human PBMCs.
METHODS: PBMCs from healthy human volunteers were cultured with E2. Levels of IgG and IgM and cytokine activity were measured by ELISA. Proliferation was determined by [3H]-thymidine uptake. The cell viability was assessed by a trypan blue exclusion test.
RESULTS: E2 enhanced IgG and IgM production of PBMCs both from men and women without altering cell viability and proliferation. The stimulatory effect of E2 was revealed at 10(-10) mol/L, increased in a dose-dependent fashion, and was maximized at 10(-8) mol/L. IgG production of PBMCs in the presence of E2 (10(-8) mol/L) was 220% of control cells, and that of IgM was 211%. Immunoglobulin production of E2 -treated B cells was slightly higher than that of control cells; IgG production was 161% of control cells, and that of IgM was 157%. Anti-IL-10 antibody partially blocked the E2 effect on immunoglobulin production of PBMCs; anti-IL-10 reduced IgG production in the presence of E2 from 206% to 154% of control cells, and that of IgM from 206% to 152%. E2 increased IL-10 production of monocytes up to 250% of control level, but it did not affect that of T cells or B cells. Exogenous IL-10 (1 U/mL) further enhanced E2 -induced increase of immunoglobulin production by B cells, although this level of IL-10 alone was ineffective for B cells.
CONCLUSION: These results suggest that E2 may increase immunoglobulin production of human PBMCs mainly by increasing IL-10 production of monocytes. The results also support that E2 may act as an important stimulator for human humoral immunity.
OBJECTIVE: We studied the in vitro effects of 17beta-estradiol (E2 ) on spontaneous immunoglobulin production by human PBMCs.
METHODS: PBMCs from healthy human volunteers were cultured with E2. Levels of IgG and IgM and cytokine activity were measured by ELISA. Proliferation was determined by [3H]-thymidine uptake. The cell viability was assessed by a trypan blue exclusion test.
RESULTS: E2 enhanced IgG and IgM production of PBMCs both from men and women without altering cell viability and proliferation. The stimulatory effect of E2 was revealed at 10(-10) mol/L, increased in a dose-dependent fashion, and was maximized at 10(-8) mol/L. IgG production of PBMCs in the presence of E2 (10(-8) mol/L) was 220% of control cells, and that of IgM was 211%. Immunoglobulin production of E2 -treated B cells was slightly higher than that of control cells; IgG production was 161% of control cells, and that of IgM was 157%. Anti-IL-10 antibody partially blocked the E2 effect on immunoglobulin production of PBMCs; anti-IL-10 reduced IgG production in the presence of E2 from 206% to 154% of control cells, and that of IgM from 206% to 152%. E2 increased IL-10 production of monocytes up to 250% of control level, but it did not affect that of T cells or B cells. Exogenous IL-10 (1 U/mL) further enhanced E2 -induced increase of immunoglobulin production by B cells, although this level of IL-10 alone was ineffective for B cells.
CONCLUSION: These results suggest that E2 may increase immunoglobulin production of human PBMCs mainly by increasing IL-10 production of monocytes. The results also support that E2 may act as an important stimulator for human humoral immunity.
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