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Published on: June 29, 2021
Antiapoptotic seminal vesicle protein IV induces histamine release from human FcepsilonRI+ cells
Nella Prevete1, Francesca Wanda Rossi, Massimo Triggiani
1Division of Clinical Immunology and Allergy, University of Naples Federico II, Naples, Italy.
Background:
Seminal vesicle protein number 4 (SV-IV) is a small, basic, multifunctional, intrinsically disordered secretory protein synthesized in large amounts by rat seminal vesicle epithelium under androgen transcriptional control. SV-IV-immunorelated proteins occur in other rat tissues and in humans.
Methods:
The in vitro effect of SV-IV on human FcepsilonRI+ cells was investigated by standard immunologic, biochemical and molecular biology procedures.
Results:
SV-IV-induced histamine release from human basophils and lung mast cells without any influence on leukotriene C(4) release and cell migration. The histamine release rate was slower compared with that induced by anti-IgE, the temperature dependence of the event being similar. SV-IV-induced histamine release was Ca2+-dependent, suggesting a physiological interaction of the protein with FcepsilonRI+ cells. SV-IV and anti-IgE acted synergistically on the histamine release. SV-IV did not induce de novo synthesis of cytokines and growth factors (transforming growth factor-beta(1), interleukin-10, interleukin-13, tumor necrosis factor-alpha, vascular endothelial growth factor A) in FcepsilonRI+ cells.
Conclusions:
SV-IV protein induces in human FcepsilonRI+ cells the release of histamine, a proinflammatory, antiapoptotic and immunosuppressive biogenic amine. These data: (1) are consistent with the antiapoptotic and immunosuppressive properties of SV-IV; (2) confirm a regulatory feature of SV-IV on mammal inflammatory reactivity by either inhibiting the arachidonate cascade pathway or stimulating proinflammatory cytokine release from lymphocyte/monocytes and histamine from FcepsilonRI+ cells; (3) raise the possibility of a protective role of SV-IV on implanting hemiallogenic blastocysts against maternal reactive oxygen species and immunological attacks at the uterine implantation site.
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