The peak plaque-forming-cell (PFC) and serum antibody responses of diabetic mice to type III pneumococcal capsular polysaccharide (S3) were delayed compared with normals. Proliferation of PFC precursors was not inhibited in an insulin-deficient environment. The delay in the PFC response to S3 did not occur in diabetic nude mice but was demonstrable in their thymus-bearing heterozygote littermates. Therefore, T-cells appear to mediate the delay in the response of diabetic mice to S3 probably by delaying their differentiation into PFC. Diabetic mice responded normally to the induction of low-dose tolerance to S3, indicating the presence of active suppressor T-cells (Ts) in these mice. However, inactivation of Ts by anti-lymphocyte serum (ALS) required a higher dose in the diabetic mice. Furthermore, inactivation of Ts by ALS totally abolished the delay in peak PFC response. These findings suggest that the delayed PFC response to S3 in diabetic mice was the result of excessive splenic Ts activity. In peripheral blood, diabetic mice appeared to have more amplifier T-cell activity or less suppressor T-cell activity than normals. This response was normalized by insulin treatment.
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February 01 1983
Impairment of T-Cell Regulation of the Humoral Immune Response to Type III Pneumococcal Polysaccharide in Diabetic Mice
Barbara E Busby;
Barbara E Busby
Division of Endocrinology, Department of Medicine, Case Western Reserve University
Cleveland, Ohio 44106
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Harvey M Rodman
Harvey M Rodman
Division of Endocrinology, Department of Medicine, Case Western Reserve University
Cleveland, Ohio 44106
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Address reprint requests to Dr. Harvey M. Rodman, Department of Medicine, Case Western Reserve University, 2074 Abington Road, Cleveland, Ohio 44106.
Diabetes 1983;32(2):156–164
Article history
Received:
May 24 1982
Revision Received:
September 03 1982
PubMed:
6219027
Citation
Barbara E Busby, Harvey M Rodman; Impairment of T-Cell Regulation of the Humoral Immune Response to Type III Pneumococcal Polysaccharide in Diabetic Mice. Diabetes 1 February 1983; 32 (2): 156–164. https://doi.org/10.2337/diab.32.2.156
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