The cellular defects possibly responsible for diminished in vivo granuloma formation in diabetic Schistosoma mansoni-infected mice were investigated. Diabetic and control animals develop a similar degree of eosinophilia. Eosinophils obtained from diabetic mice also respond normally to the lymphokine eosinophil stimulation promoter (ESP). Lymphoid cells of chemically induced (streptozotocin) and mutation diabetic (db/db) mice, however, have a decreased capacity to produce/secrete ESP in response to soluble egg antigens of S. mansoni. Administration of insulin to diabetic mice is associated with a partial reversal of the decreased ability of their lymphoid cells to generate ESP. These findings show that defective cellular immunity in diabetic animals may be partially explained by the failure of their lymphocytes to produce the soluble mediators involved in recruitment of target cells.


This work was supported by the National Cancer Institute Grant CA-05851, the Rockefeller Foundation Grant GA HS 7801, the United States Public Health Service Grants AI-15351, AM-21259, and RR080, and by grants from the Diabetes Association of Greater Cleveland, the American Diabetes Association, and the Juvenile Diabetes Foundation.

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