Defective Resistance to Plasmodium Yoelii in CBA/N Mice

Abstract

The role of B lymphocytes in resistance to malaria was studied in defective and normal F₁ mice derived from CBA/N mice, a strain with an X-linked B cell defect. When infected with normally nonlethal Plasmodium yoelii, immune defective F₁ male mice had higher parasitemias and more prolonged infections than normal F₁ mice, as well as a 50% mortality rate. Before infection the plasma levels of IgM and IgG were lower in defective F₁ males than normal F₁ mice. The polyclonal IgM and IgG responses of infected abnormal F₁ mice were delayed and lower in absolute magnitude than those of normal F₁ mice. Furthermore, specific IgM and IgG anti-plasmodial antibody titers, as determined by radioimmunoassay, were depressed on day 12 in the defective F₁ males. Although IgG titers approached those of the normal F₁ mice on day 19, defective F₁ male IgM titers remained depressed. These data demonstrate that an X-linked gene that affects B cell function influences malarial resistance in mice, presumably via a decreased specific IgM response, and the slow development of a specific IgG response to P. yoelii infection.