Reduced response of splenocytes after mitogen-stimulation in the prion protein (PrP) gene-deficient mouse: PrPLP/Doppel production and cerebral degeneration
- Department of Molecular Immunology, School of Agricultural and Life Sciences, University of Tokyo, Bunkyo-ku, Tokyo 113-8657 (Japan)
- Department of Internal Medicine, College of Veterinary Medicine and Institute of Animal Medicine, Gyeongsang National University, Chinju 660-701 (Korea, Republic of)
- Laboratory for Behavioral Genetics, Brain Science Institute, RIKEN, Wako, Saitama 351-0198 (Japan)
- Department of Molecular Microbiology, Nagasaki University Graduate School of Biomedical Sciences, Sakamoto, Nagasaki 852-8523 (Japan)
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.
- OSTI ID:
- 20991409
- Journal Information:
- Biochemical and Biophysical Research Communications, Vol. 358, Issue 2; Other Information: DOI: 10.1016/j.bbrc.2007.04.174; PII: S0006-291X(07)00870-4; Copyright (c) 2007 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
- Country of Publication:
- United States
- Language:
- English
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