Using female BALB/c mice, 8 weeks of age, and group A streptococcus, Type 3 (strain B 930/24/3), experimental studies were carried out. Mice were divided into two groups; to one of the groups, heat-killed bacteria (2×10^8/ml) were injected intravenously (i.v. group) and to the other one, living cells (2×10^8/ml) were inoculated subcutaneously (s.c. group). The protein components and C-polysaccharide extracted from streptococcal cell walls were used as antigens. The humoral antibody titers against these antigens were measured by passive hemagglutination technique, and the delayed-type hypersensitivity (DTH) of the sensitized mice was tested by foodpad reaction. The production of humoral antibody was found in the sera of the i.v. group, but DTH was not induced in mice of this group. In mice of the s.c. group, the DTH to streptococcal protein components was positive and the antibody titers against these antigens were of at low levels. However, pathological changes of kidney were not observed in either the i.v. or the s.c. group. The lymphocytes obtained from the s.c. group were transferred into the i.v. group, and then the fragments of ultrasonic distrupture of heat-killed bacteria (transfer group) were injected intravenously to the mice. On light microscopic findings on these mice, the glomerulus showed segmental hypercellularity with proliferation of mesangial matrix, and in electron microscopic findings, the glomerulus showed swelling of endothelium and proliferation of mesangial matrix. The lymphocytes treated with anti-thymocyte serum and complement were transferred into the i.v. group. However, the pathological changes in the glomerulus were not observed in these mice. These findings suggest that pathological changes in experimental nephritis of mice may be induced by interaction of humoral and cellular immunity.
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