Lactic dehydrogenase virus infection prevents development of anti-nuclear antibody in (NZB x NZW)F1 mice; role of prostaglandin E2 and macrophage Ia antigen expression.
Persistent lactic dehydrogenase virus (LDV) infection prevents the development of antinuclear antibody (ANA) in (NZB x NZW)F1 mice. To assess the suppressive mechanisms, we focused on the role of the E series of prostaglandin(PGE), since previously we have shown enhanced production of PGE by macrophages from chronically LDV-infected mice. Treatment with PGE2 suppressed ANA titres more markedly in non-infected mice than in LDV-infected mice. Indomethacin enhanced ANA titres more markedly in LDV-infected mice than in non-infected mice. The number of Ia antigen positive(Ia+) macrophages was less in LDV-infected mice than in uninfected mice. The number of Ia+ macrophages was decreased in non-infected mice by PGE2 treatment and increased in LDV-infected mice by indomethacin treatment. These results suggest that the low ANA production in LDV-infected (NZB x NZW)F1 mice may be related to the decreased number of Ia+ macrophages and that one of the factors responsible for suppression of Ia+ macrophages may be the enhanced PGE2 production in the LDV-infected mice.
Hayashi
T
T
Laboratory of Veterinary Pathology, University of Yamaguchi, Japan.
Mori
I
I
Yamamoto
H
H
D000818:Animals; D000974:Antibodies, Antinuclear / Q000096:biosynthesis*; D002452:Cell Count; D015232:Dinoprostone / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis*; D007108:Immune Tolerance; D007213:Indomethacin / Q000494:pharmacology; D007772:Lactate dehydrogenase-elevating virus / Q000276:immunology*; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008815:Mice, Inbred Strains; D013997:Time Factors; D014777:Virus Diseases / Q000276:immunology*
D000974:Antibodies, Antinuclear; D000949:Histocompatibility Antigens Class II; D015232:Dinoprostone; D007213:Indomethacin