Effect of PGE1 treatment on in vitro thymocyte function of normal and autoimmune mice.
Autoimmune New Zealand (NZ) mice exhibit a broad spectrum of T and B cell disorders. These include abnormally high levels of terminal deoxynucleotidyl transferase-positive immature T cells in bone marrow and thymus. We have shown previously that prostaglandin E1 (PGE1) treatment of the NZB/NZW F1 hybrid, a murine model of systemic lupus erythematosus (SLE), reduces to normal the percentage of immature terminal deoxynucleotidyl transferase-positive cells in bone marrow and thymus, and prevents the immune complex-induced nephritis which kills these animals. We report here that short-term (1-5 days) treatment of NZB/W mice with PGE1 increases thymocyte responsiveness to mitogens and alloantigens. The majority (greater than 90%) of cortical thymocytes agglutinated by peanut lectin (PNA+) are depleted by PGE1 treatment. However, a small population of highly functional cells persists in the PNA+ fraction after PGE1 treatment. PGE1 appears to have little or no effect on the PNA-negative (medullary) fraction of thymocytes. Our data suggest that PGE1 may exert its therapeutic effect in NZ mice by increasing the functional maturity of immature T cells.
Whittum-Hudson
J
J
Department of Pathology, University of Connecticut Health Center, School of Medicine, Farmington 06032.
Ballow
M
M
Zurier
R B
RB
D000305:Adrenal Cortex Hormones / Q000494:pharmacology; D000527:Alprostadil / Q000494:pharmacology*; D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology*; D066298:In Vitro Techniques; D008213:Lymphocyte Activation / Q000187:drug effects; D007959:Lymphocyte Culture Test, Mixed; D051379:Mice; D008934:Mitogens / Q000494:pharmacology; D013601:T-Lymphocytes / Q000187:drug effects* / Q000276:immunology
D000305:Adrenal Cortex Hormones; D008934:Mitogens; D000527:Alprostadil