Comparative analysis of normal prion protein expression on human, rodent, and ruminant blood cells by using a panel of prion antibodies

被引:32
作者
Barclay, GR [1 ]
Houston, EF
Halliday, SI
Farquhar, CF
Turner, ML
机构
[1] Western Gen Hosp, John Hughes Bennett Lab, Scottish Natl Blood Transfus Serv Cell Therapy Gr, Edinburgh EH4 2XU, Midlothian, Scotland
[2] Inst Anim Hlth, Neuropathogenesis Unit, Edinburgh, Midlothian, Scotland
关键词
D O I
10.1046/j.1537-2995.2002.00095.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BACKGROUND: It is not known whether variant CJD can be transmitted within the human population by blood transfusion. The expression of normal cellular prion protein (PrPC) by different blood cell types may permit selective uptake and dissemination of infectivity. STUDY DESIGN AND METHODS: The normal distribution of PrPC on the major blood cell types of species known to be susceptible to natural or experimental transmissible spongiform encephalopathies was studied. Blood from healthy humans, mice, hamsters, cattle, and sheep was examined by flow cytometry by using a large panel of antibodies with different prion protein (PrP) epitope specificities to maximize the detection of PrP variants across species and cell type. RESULTS: PrP was detected on all major human blood cells types except eosinophils, but was not detected as ubiquitously or uniformly on major blood cell types of different animal species. CONCLUSION: Different animal species have unique patterns of expression of PrPC on blood cell types, with none equivalent to the human pattern. This needs to be considered when extrapolating from animal models of blood-borne transmissible spongiform encephalopathy infectivity, particularly in regard to the risk assessment of potential variant CJD spread within the human population. The relationship between PrP distribution and infectivity distribution in blood needs further investigation.
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收藏
页码:517 / 526
页数:10
相关论文
共 64 条
[31]  
3.0.CO
[32]  
2-Z
[33]   MOUSE POLYCLONAL AND MONOCLONAL-ANTIBODY TO SCRAPIE-ASSOCIATED FIBRIL PROTEINS [J].
KASCSAK, RJ ;
RUBENSTEIN, R ;
MERZ, PA ;
TONNADEMASI, M ;
FERSKO, R ;
CARP, RI ;
WISNIEWSKI, HM ;
DIRINGER, H .
JOURNAL OF VIROLOGY, 1987, 61 (12) :3688-3693
[34]   Immunodiagnosis of prion disease [J].
Kascsak, RJ ;
Fersko, R ;
Pulgiano, D ;
Rubenstein, R ;
Carp, RI .
IMMUNOLOGICAL INVESTIGATIONS, 1997, 26 (1-2) :259-268
[35]   Generation of monoclonal antibodies against human prion proteins in PrP0/0 mice [J].
Krasemann, S ;
Groschup, MH ;
Harmeyer, S ;
Hunsmann, G ;
Bodemer, W .
MOLECULAR MEDICINE, 1996, 2 (06) :725-734
[36]   CREUTZFELDT-JAKOB DISEASE IN MICE - PERSISTENT VIREMIA AND PREFERENTIAL REPLICATION OF VIRUS IN LOW-DENSITY LYMPHOCYTES [J].
KURODA, Y ;
GIBBS, CJ ;
AMYX, HL ;
GAJDUSEK, DC .
INFECTION AND IMMUNITY, 1983, 41 (01) :154-161
[37]  
LANGEVELD JPM, 1994, BSE UPDATE, P315
[38]   Augmentation in expression of activation-induced genes differentiates memory from naive CD4+ T cells and is a molecular mechanism for enhanced cellular response of memory CD4+ T cells [J].
Liu, K ;
Li, Y ;
Prabhu, V ;
Young, L ;
Becker, KG ;
Munson, PJ ;
Weng, NP .
JOURNAL OF IMMUNOLOGY, 2001, 166 (12) :7335-7344
[39]  
Liu T, 2001, J IMMUNOL, V166, P5840
[40]   Involvement of the immune system in TSE pathogenesis [J].
Mabbott, NA ;
Farquhar, CF ;
Brown, KL ;
Bruce, ME .
IMMUNOLOGY TODAY, 1998, 19 (05) :201-203