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Defective Resistance to Plasmodium Yoelii in CBA/N Mice¹

From the Department of Internal Medicine, Uniformed Services University of the Health Sciences and the Department of Immunology, Naval Medical Research Institute, Bethesda, Maryland 20014

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.

Footnotes

¹ This work was supported by the Uniformed Services University of the Health Sciences Protocol No. RO8305 and the Naval Medical Research and Development Command, Work Unit No. M0095-PN.001-1030. The opinions or assertions contained herein are the private ones of the authors and are not to be construed as official or reflecting the views of the Department of Defense, the United States Navy Department or the naval service at large. The experiments reported herein were conducted according to the principles set forth in the "Guide for the Care and Use of Laboratory Animals," Institute of Laboratory Animal Resources, National Research Council, DHEW Pub. No. (NIH) 74-23.