학술논문
Reduced response of splenocytes after mitogen-stimulation in the prion protein (PrP) gene-deficient mouse: PrPLP/Doppel production and cerebral degeneration
Document Type
Author abstract
Author
Source
Biochemical and Biophysical Research Communications. June 29, 2007, Vol. 358 Issue 2, p469, 6 p.
Subject
Language
English
ISSN
0006-291X
Abstract
To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.bbrc.2007.04.174 Byline: Chi-Kyeong Kim (a), Yuko Hirose (a), Akikazu Sakudo (a), Natsumi Takeyama (a), Chung-Boo Kang (b), Yojiro Taniuchi (a), Yoshitsugu Matsumoto (a), Shigeyoshi Itohara (c), Suehiro Sakaguchi (d)(e), Takashi Onodera (a) Keywords: Prion disease; Prion protein; Apoptosis; PrP-deficient mice; Spleen Abstract: Splenocytes of wild-type (Prnp.sup.+/+) and prion protein gene-deficient (Prnp.sup.-/-) mice were treated with various activation stimuli such as T cell mitogen concanavalin A (ConA), phorbol 12-myristate 13-acetate (PMA)+ionomycin (Io), or B cell mitogen lipopolysaccharide (LPS). Cellular prion protein (PrP.sup.C) expression was enhanced following ConA stimulation, but not PMA+Io or LPS in Prnp.sup.+/+ splenocytes. Rikn Prnp.sup.-/- splenocytes elicited lower cell proliferations than Prnp.sup.+/+ or Zrch I Prnp.sup.-/- splenocytes after LPS stimulation and showed sporadic nerve cells in the cerebral cortex and deeper structure. Around the degenerated nerve cells, mild vacuolation in the neuropil was observed. This neural alteration correlated well to the suppressed response of B cells in the spleen. The finding that discrete lesions within the central nervous systems induced marked modulation of immune function probably indicates the existence of a delicately balanced neural-endocrine network by PrP.sup.C and PrPLP/Doppel. Author Affiliation: (a) Department of Molecular Immunology, School of Agricultural and Life Sciences, University of Tokyo, Bunkyo-ku, Tokyo 113-8657, Japan (b) Department of Internal Medicine, College of Veterinary Medicine and Institute of Animal Medicine, Gyeongsang National University, Chinju 660-701, Republic of Korea (c) Laboratory for Behavioral Genetics, Brain Science Institute, RIKEN, Wako, Saitama 351-0198, Japan (d) Department of Molecular Microbiology, Nagasaki University Graduate School of Biomedical Sciences, Sakamoto, Nagasaki 852-8523, Japan (e) Department of Immunology, Nagasaki University Graduate School of Biomedical Sciences, Sakamoto, Nagasaki 852-8523, Japan Article History: Received 18 April 2007