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T‐lymphocyte activation and the cellular form of the prion protein
Author(s) -
MABBOTT N. A.,
BROWN K. L.,
MANSON J.,
BRUCE M. E.
Publication year - 1997
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1997.00331.x
Subject(s) - scrapie , biology , bovine spongiform encephalopathy , concanavalin a , lymphocyte , in vitro , stimulation , glycoprotein , microbiology and biotechnology , cell , central nervous system , immune system , immunology , virology , prion protein , genetics , neuroscience , disease , pathology , medicine
The transmissible spongiform encephalopathies are neurodegenerative disorders which include Creutzfeldt–Jakob disease in humans, and scrapie and bovine spongiform encephalopathy in animals. A major component of the infectious agent responsible for these diseases is considered to be a post‐translationally modified form of a host‐encoded glycoprotein PrP c , termed PrP Sc . While PrP c is abundantly expressed in tissues of the central nervous system (CNS), little is known about its normal function. The expression of PrP c is not restricted to the CNS, as this protein can also be detected in the lymphoid tissues of mice and sheep. In this report we demonstrate that resting murine splenic lymphocytes express PrP c protein on their cell membranes. Furthermore, expression of PrP c was significantly enhanced following in vitro stimulation with the non‐specific T‐cell mitogen concanavalin A (Con A). Genetically engineered mice with an inactive PrP c gene (PrP −/− mice), were utilized to investigate the involvement of PrP c in lymphocyte activation. Experiments revealed that the Con A‐induced proliferation of lymphocytes from PrP −/− mice was significantly reduced to ≈50–80% that of wild‐type (PrP +/+ ) mice 48 hr post‐stimulation. These findings demonstrate an important role for PrP c in extra‐neuronal tissues and suggest that PrP c is a lymphocyte surface molecule that participates in T‐cell activation.