Physiology of IgD III. Effect of treatment with anti-IgD from birth on the magnitude and isotype distribution of the immune response in the spleen

Abstract

Continued treatment with monoclonal anti‐IgD (Ig‐5a) from birth in BALB/c mice causes a markedly increased responsiveness to i.v. injected dinitrophenylated ovalbumin (DNP‐OVA) with Bordetella pertussis at the age of 8 weeks. The 19 S plaqueforming cell (PFC)/spleen response is particularly enhanced, 6–8‐fold, but all the other isotypes also show increases of 2–6‐fold, including IgA and IgE. Both primary and secondary PFC responses and serum antibody titers are enhanced. After transfer of spleen cells from anti‐Ig‐treated mice to irradiated recipients the IgM/IgG ratio becomes similar to that of controls. In contrast, the response of anti‐IgD‐treated mice to i.p. immunization with either 0.2 or 100 μg DNP‐OVA plus alum is reduced by approximately 80% for each Ig isotype except IgM and remains low upon transfer of spleen cells to recipients. It is concluded that the paucity of B cells in peripheral lymph nodes of the anti‐IgD‐treated mice causes the low responsiveness to i.p. immunization, but that the IgD⁻ B cells in the spleen are quite able to respond and are, in fact, more responsive than IgD⁺ B cells. This increased responsiveness, together with the higher IgM/IgG ratios for all Ig isotypes and an otherwise similar order of isotype distribution (γ₁ > γ_2b > γ_2a = ϵ ≧ α) as in controls, suggests that a hyperresponsive, but less mature IgD⁻ B cell population is selectively produced in the spleens of mice treated with anti‐IgD from birth.