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IL-6 Knock-Out Mice Show Modified Basal Immune Functions, but Normal Immune Responses to Stress

To better determine the role of interleukin-6 in the mechanisms that regulate stress-induced immunosuppression, we used in this study an interleukin-6-deficient mice model recently generated by gene targeting. We report here that, in basal conditions, mutant mice are characterized by altered immune...

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Bibliographic Details
Published in:Brain, behavior, and immunity behavior, and immunity, 1998-09, Vol.12 (3), p.201-211
Main Authors: Manfredi, Barbara, Sacerdote, Paola, Gaspani, Leda, Poli, Valeria, Panerai, Alberto E.
Format: Article
Language:English
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Summary:To better determine the role of interleukin-6 in the mechanisms that regulate stress-induced immunosuppression, we used in this study an interleukin-6-deficient mice model recently generated by gene targeting. We report here that, in basal conditions, mutant mice are characterized by altered immune functions. Natural killer activity and interleukin-2 production are lower in splenocytes of interleukin-6 deficient mice compared to those of controls, whereas Concanavalin A-induced splenocyte proliferation is comparable with that observed in wild-type mice. Moreover, splenocyte concentrations of the immunosuppressive opioid peptide β-endorphin are higher in interleukin-6 deficient mice while serum corticosterone concentrations are unchanged. After exposure to 16 h of restraint stress, a significant suppression of the immune parameters is exhibited and a significant increase of splenocyte β-endorphin concentrations are present in knock-out and normal animals. Finally, corticosterone is normally induced in stressed interleukin-6-deficient mice, thus demonstrating that interleukin-6 is not crucial for the activation of the hypothalamic–pituitary–adrenal axis. In conclusion, our results indicate that interleukin-6 is not a key factor in the immunosuppression observed after restraint stress.
ISSN:0889-1591
1090-2139
DOI:10.1006/brbi.1998.0525