1. Splenic macrophages and B cells mediate immunosuppression following abrupt withdrawal from morphine.
- Author
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Rahim RT, Meissler JJ Jr, Adler MW, and Eisenstein TK
- Subjects
- Acute Disease, Animals, Antigens, CD19 immunology, B-Lymphocytes drug effects, CD11 Antigens immunology, Cell Proliferation drug effects, Cells, Cultured, Coculture Techniques, Concanavalin A pharmacology, Disease Models, Animal, Female, Immune Tolerance drug effects, Immunomagnetic Separation, Inflammation Mediators pharmacology, Lipopolysaccharides pharmacology, Macrophages drug effects, Mice, Mice, Inbred C3H, Morphine adverse effects, Morphine Dependence physiopathology, Narcotics adverse effects, Spleen physiopathology, Substance Withdrawal Syndrome physiopathology, B-Lymphocytes immunology, Immune Tolerance immunology, Macrophages immunology, Morphine Dependence immunology, Spleen immunology, Substance Withdrawal Syndrome immunology
- Abstract
We have previously shown that abrupt withdrawal (AW) from morphine induces greater than 80% immunosuppression in murine spleen cells, as assessed by the capacity to mount an in vitro plaque-forming cell response to sheep red blood cells. Present studies about the mechanisms of immunosuppression following AW showed that addition of highly enriched (CD11b+) splenic macrophages (obtained by cell sorting or magnetic separation) from AW mice to cultures of normal, unfractionated spleen cells suppressed immune responses. Further, addition of highly enriched (CD19+) B cells (but not T cells) from AW mice to normal cells was also immunosuppressive. B cells from AW mice were also able to inhibit the proliferative response of normal spleen cells to concanavalin A but not to lipopolysaccharide. Overall, the data suggest that immunosuppression by AW spleen cells is a result of active suppression by macrophages and B cells.
- Published
- 2005
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