Polyclonal B cell activation of IgG2a and IgG2b production by infection of mice with lactate dehydrogenase-elevating virus is partly dependent on CD4+ lymphocytes.

作者: XIN LI , BUGEN HU , JOHN HARTY , CHEN EVEN , PETER G.W. PLAGEMANN

DOI: 10.1089/VIM.1990.3.273

关键词:

摘要: Concentrations of IgM and IgG isotypes were determined by capture ELISA in plasma Swiss, BALB/c C58/M mice. Plasma isotype concentrations, especially IgM, IgG1 IgG2a, varied considerably between mouse strains, batches mice the same strain individual as a function age. Infection with LDV, which is known to replicate primarily subpopulation macrophages, consistently resulted rapid elevation IgG2a (or IgG2b some Swiss nu/+ mice), but no increases observed immunized inactivated LDV. after LDV infection was greatly delayed reduced depletion CD4+, not CD8+, T cells administration protein-G-purified anti-CD4 or anti-CD8 mAbs, completely inhibited repeated treatment cyclophosphamide. Treatment cyclophosphamide also production anti-LDV antibodies, while significantly affecting replication these Nude failed produce though supporting normal replication. IgG1, levels increased LDV-infected nu/nu mice, similar changes uninfected The results indicate that LDV-induced polyclonal activation B requires productive is, at least partly, dependent on functioning CD4+ cells. They suggest LDV-permissive macrophages leads lymphocytes subset 1 their Spleen from 5-day incorporated [3H]thymidine 2-3 times more rapidly vitro than spleen companion whereas responses concanavalin A lipopolysaccharide 60-70%.

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