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The Journal of Immunology, 1979, 123: 660-666.
Copyright © 1979 by The American Association of Immunologists, Inc.

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Autoimmune Cell-Mediated Responses: Spontaneous Responses to Syngeneic Cells in NZB/NZW F1 Mice1

David Senitzer, William Cafruny2, Roberta Raeder and Earl H. Freimer

From the Departments of Microbiology and Medicine, Medical College of Ohio, C. S. 10008, Toledo, Ohio 43699

Abstract

The effect of various stimulator cell populations on B/W mouse spleen cell cultures was analyzed by measuring 3H-thymidine incorporation. The data show that syngeneic heart and kidney cells induce strong stimulation of DNA synthesis in B/W spleen cells. In contrast, syngeneic liver cells are not stimulatory. Autologous stimulation of adult B/W spleen cells by heart and kidney cells was also observed. BALB/c heart and kidney cells were stimulatory for B/W spleen cells, although BALB/c spleen cells were only slightly stimulated by B/W or BALB/c heart and kidney cells.

The responses to syngeneic heart and kidney cells were observed to peak at 7 to 8 days of culture. The magnitude of the observed responses did not appear to correlate with the age or sex of the B/W spleen cells used, and the ability to response to heart and kidney cells with large increases in DNA synthesis occurred at a very early age. Spleen cells from old B/W mice lose the ability to become stimulated by concanavalin A, although no concomitant loss of reactivity to syngeneic heart or kidney cells is observed. The presence of {theta}-bearing lymphocytes in B/W spleen cell populations is not required during culture initiation for the stimulation of DNA synthesis by syngeneic heart or kidney cells. However, during the peak of DNA synthesis, the majority of responder spleen cells carry {theta}-antigen.

We postulate that antigenic determinants present on heart and kidney cells induce in vitro cell-mediated immune responses of an autoimmune nature in B/W spleen cell populations. The results are in aggrement with an early defect in immunologic regulation that persists throughout the life of the B/W mouse.

Footnotes

1 This work was supported in part by grants from the Lupus Society of the Northwest Ohio branch of the Arthritis Foundation, the Mather Fund, and Biomedical Research Grant 5-507-RR-05700-08.

2 In partial fulfillment of requirements for the doctoral degree.







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