receiving information from the immune system. It remains to be determined, however, whether the nervous system is capable of acting upon that information. In the present instance, the source and nature of the cues that signal a dysregulated immune system remain to be determined. Also, it remains to be determined whether the lupus-prone animal is responding to CY-induced changes in immune function, per se, or the effects of CY in normalizing some other specific or nonspecific physiological effect(s) of the autoimmune disease. The data described here suggest that lupus-prone MRL-lpr/lpr mice are not responding to their lymphadenopathy or to their elevated autoantibody titers.
Whatever the immediate source of the signals that are motivating the observed changes in behavior, the primary defect of these lupus-prone animals is immunologic. These results thus provide additional evidence for CNS-immune system interactions. Consistent with previous observations, these results also illustrate and extend the role of learning in the regulation of physiological states and raise the interesting possibility that there are circumstances under which behavior can serve an in vivo immunoregulatory function.
This chapter constituted part of the Salmon Lecture delivered at the New York Academy of Medicine, December 7, 1989. The author's research was supported by a Research Scientist Award (K3 MH06318) from the National Institute of Mental Health and by Research Grants from the National Institute for Neurological and Communicative Diseases and Stroke (NS22228) and from RJR Nabsico, Inc.
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Publication information: Book title: Stress and Disease Processes. Contributors: Neil Schneiderman - Editor, Philip McCabe - Editor, Andrew Baum - Editor. Publisher: Lawrence Erlbaum Associates. Place of publication: Hillsdale, NJ. Publication year: 1992. Page number: 101.
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