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Effect of female sex steroids on splenocyte ability to produce an adoptive immune response. Role of prostaglandin F2a in hormonal immunoregulation mechanisms

https://doi.org/10.14341/probl12018

Abstract

Male CBA mice were used in experiments. Splenocytes were incubated for an hour in macrocultures with estradiol (E2) or progesterone (P), then the cells were transferred (together with the antigen) to lethally irradiated syngeneic recipients, and on day 4 the count of antibody-producing cells (APC) was estimated. Prostaglandin F2a (PGF2a) concentrations were radioimmunoassayed in cell culture supernatants. E2 and P concentrations corresponded to these hormones levels in blood sera during pregnancy. E2 and P in the tested concentrations were found to reliably stimulate the processes of APC formation, their effects being dose independent. Both E2 and P statistically reliably increased PGF2a level in splenocyte culture. Fractionation of splenocytes helped reveal the highest PGF2a level in the cultures devoid of adhesive cells and rich for T lymphocytes. Hence, E2 and P stimulated the processes of antigen-independent differentiation of splenocytes producing APC either by directly stimulating T lymphocytes or via macrophages by blocking their negative effects. Stimulation of adoptive immune response by sex steroids is closely connected with PGF2a production by immunocompetent cells under the effects of these hormones.

About the Authors

S. V. Shirshev
Ecology and Microorganism Genetics Institute
Russian Federation


Yu. I. Shilov
Ecology and Microorganism Genetics Institute
Russian Federation


N. N. Kevorkov
Ecology and Microorganism Genetics Institute
Russian Federation


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Review

For citations:


Shirshev S.V., Shilov Yu.I., Kevorkov N.N. Effect of female sex steroids on splenocyte ability to produce an adoptive immune response. Role of prostaglandin F2a in hormonal immunoregulation mechanisms. Problems of Endocrinology. 1994;40(3):47-49. (In Russ.) https://doi.org/10.14341/probl12018

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ISSN 0375-9660 (Print)
ISSN 2308-1430 (Online)