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Induction of Apoptosis in Thymocytes by Prostaglandin E(2) In Vivo

In vivo administration in mice of a synthetic analog of prostaglandin E(2) (PGE(2)) caused a selective and dramatic decrease of CD4(+)CD8(+) double-positive, CD3/T-cell-receptor-αb(10) cells in the thymus. This loss was corticosteroid-independent and not affected by Cyclosporin A. The disappearance...

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Detalles Bibliográficos
Autores principales: Mastino, Antonio, Piacentini, Mauro, Grelli, Sandro, Favalli, Cartesio, Autuori, Francesco, Tentori, Lucio, Oliverio, Serafina, Garach, Enrico
Formato: Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 1992
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2275867/
https://www.ncbi.nlm.nih.gov/pubmed/1364176
http://dx.doi.org/10.1155/1992/80863
Descripción
Sumario:In vivo administration in mice of a synthetic analog of prostaglandin E(2) (PGE(2)) caused a selective and dramatic decrease of CD4(+)CD8(+) double-positive, CD3/T-cell-receptor-αb(10) cells in the thymus. This loss was corticosteroid-independent and not affected by Cyclosporin A. The disappearance of CD4(+)CD8(+) thymocytes was strictly correlated with the induction of apoptosis inside the thymus as shown by morphological studies and by the induction of intracellular transglutaminase expression. Considering that PGE(2) has been found to be produced by different cell populations inside the thymus, these results indicate that PGE(2) may act as endogenous signals for apoptosis during T-cell differentiation.