NR AXCB
AU Kim,C.K.; Hirose,Y.; Sakudo,A.; Takeyama,N.; Kang,C.B.; Taniuchi,Y.; Matsumoto,Y.; Itohara,S.; Sakaguchi,S.; Onodera,T.
TI Reduced response of splenocytes after mitogen-stimulation in the prion protein (PrP) gene-deficient mouse: PrPLP/Doppel production and cerebral degeneration.
QU Biochemical and Biophysical Research Communications 2007 Jun 29; 358(2): 469-74
PT journal article; research support, non-u.s. gov't
AB Splenocytes of wild-type (Prnp(+/+)) and prion protein gene-deficient (Prnp(-/-)) 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 (PrPc) expression was enhanced following ConA stimulation, but not PMA+Io or LPS in Prnp(+/+) splenocytes. Rikn Prnp(-/-) splenocytes elicited lower cell proliferations than Prnp(+/+) or Zrch I Prnp(-/-) 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 PrPc and PrPLP/Doppel.
MH Animals; Cerebral Cortex/drug effects/*metabolism/*pathology; Lymphocytes/drug effects/*metabolism/*pathology; Mice; Mice, Knockout; Mitogens/*pharmacology; Prions/genetics/*metabolism
AD Department of Molecular Immunology, School of Agricultural and Life Sciences, University of Tokyo, Tokyo, Japan.
SP englisch
PO USA