Central interferon-α inhibits natural killer cytotoxicity through sympathetic innervation

Sachiko Take, T. Mori, T. Katafuchi, T. Hori

Research output: Contribution to journalArticle

59 Citations (Scopus)

Abstract

The brain has been known to produce high levels of interferon-α (IFN-α) during viral infections. We investigated the central and peripheral mechanisms of the brain IFN-α-induced suppression of natural killer (NK) cytotoxicity in the rat. The activity of NK cells in the spleen and the peripheral blood decreased 30-120 min after intracerebroventricular (icv) injection of recombinant human IFN-α of >1,000 U but not after its intraperitoneal injection. This effect was antagonized by pretreatment with icv naltrexone (NLTX). Splenic denervation was observed to completely abolish the IFN-α-induced suppression of NK activity, whereas bilateral adrenalectomy did not. Furthermore, this immunosuppression was blocked by an icv injection of an antagonist of corticotropin-releasing factor (CRF), α- helical CRF-(9-41). The icv injection of CRF resulted in reduced NK activity, which was not affected by NLTX. The results suggest that brain IFN-α activates the CRF system through central opioid receptors and thereby suppresses the NK cytotoxicity predominantly through splenic sympathetic innervation.

Original languageEnglish
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume265
Issue number2 34-2
Publication statusPublished - Jan 1 1993

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Interferons
Corticotropin-Releasing Hormone
Naltrexone
Injections
Brain
Adrenalectomy
Opioid Receptors
Denervation
Virus Diseases
Intraperitoneal Injections
Natural Killer Cells
Immunosuppression
Spleen

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

Central interferon-α inhibits natural killer cytotoxicity through sympathetic innervation. / Take, Sachiko; Mori, T.; Katafuchi, T.; Hori, T.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 265, No. 2 34-2, 01.01.1993.

Research output: Contribution to journalArticle

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