The immunobiology of TSE diseases

Mabbott, Neil A.; Bruce, Moira E.

doi:10.1099/0022-1317-82-10-2307

Cited by 73 publications

(45 citation statements)

References 99 publications

(198 reference statements)

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“…The complement system appears to play an important role in early TSE pathogenesis (Mabbott and Bruce, 2001;Flores-Langarica et al, 2009 disease. These data are the first characterization of genes associated with the complement system in white-tailed deer and the first assessment of the role of complement gene polymorphism in TSE susceptibility.…”

Section: Discussionmentioning

confidence: 99%

“…These early stages of peripheral TSE infection including PrP Sc invasion, dissemination, and replication likely involve activation of the complement system . Support for complement system involvement in early stages of TSE disease came from studies demonstrating impeded accumulation of PrP Sc in lymphoid tissue and delayed spread of disease to the brain in mice deficient in C3 or C1q (Klein et al, 2001;Mabbott and Bruce, 2001 Botto et al, 1990;Petry et al, 1996;Moulds et al, 2001). Some of these polymorphisms have been associated with disease susceptibility or progression (e.g., Petry et al, 1995;Messias-Reason et al, 2003;Cockburn et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms

Blanchong

Heisey

Scribner

et al. 2009

Infection, Genetics and Evolution

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The genetic basis of susceptibility to chronic wasting disease (CWD) in free-ranging cervids is of great interest. Association studies of disease susceptibility in free-ranging populations, however, face considerable challenges including: the need for large sample sizes when disease is rare, animals of unknown pedigree create a risk of spurious results due to population admixture, and the inability to control disease exposure or dose. We used an innovative matched case-control design and conditional logistic regression to evaluate associations between polymorphisms of complement C1q and prion protein (Prnp) genes and CWD infection in white-tailed deer from the CWD endemic area in southcentral Wisconsin. To reduce problems due to admixture or disease-risk confounding, we used neutral genetic (microsatellite) data to identify closely related CWD-positive (n = 68) and CWD-negative (n = 91) female deer to serve as matched cases and controls. Cases and controls were also matched on factors (sex, location, age) previously demonstrated to affect CWD infection risk. For Prnp, deer with at least one Serine (S) at amino acid 96 were significantly less likely to be CWD-positive relative to deer homozygous for Glycine (G). This is the first characterization of genes associated with the complement system in white-tailed deer. No tests for association between any C1q polymorphism and CWD infection were significant at p < 0.05. After controlling for Prnp, we found weak support for an elevated risk of CWD infection in deer with at least one Glycine (G) at amino acid 56 of the C1qC gene. While we documented numerous amino acid polymorphisms in C1q genes none appear to be strongly associated with CWD susceptibility.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms

Blanchong

Heisey

Scribner

et al. 2009

Infection, Genetics and Evolution

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“…PrPd accumulates inside the germinal centres (McBride et al, 1992) before spreading to the sites of neuroinvasion. The cells implicated in prion pathogenesis are follicular dendritic cells (FDCs) which reside in the germinal centre (Jeffrey et al, 2000;Mabbott and Bruce, 2001). Numerous studies using chimaeric mice indicate that mature follicular dendritic cells are necessary for prion propagation within the lymphoreticular system (Brown et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Features of follicular dendritic cells in ovine pharyngeal tonsil: An in vivo and in vitro study in the context of scrapie pathogenesis

Toppets

Defaweux

Piret

et al. 2011

Veterinary Immunology and Immunopathology

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a b s t r a c tAlthough the alimentary tract has been suggested as the most likely portal of entry in natural scrapie, a growing amount of data indicates that the respiratory system and more specifically the pharyngeal tonsils serve as a natural portal of entry for scrapie.This study describes for the first time the broad cell populations in the lymphoid compartment of pharyngeal tonsils and more specifically inside the lymphoid follicles where the scrapie agent accumulates during the period of latency.Follicular dendritic cells (FDCs), stromal cells located in the light zone of the germinal centre of lymphoid follicles, seem to be the principal causal factor in the accumulation of the infectious agent in transmissible spongiform encephalopathy (TSE) diseases. Knowing that efficient lymphoreticular prion propagation requires PrPc expression, we analysed the expression of PrPc with the mouse monoclonal antibody Pri 909 both in situ and on FDC-cluster-enriched cell suspensions.In situ, a positive staining was observed in the germinal centre of pharyngeal lymph follicles. The germinal centre labelling was due to the presence of a follicular dendritic network as revealed after immunogold staining of isolated FDC clusters. Our results suggest that the pharyngeal lymphoreticular system and more specifically PrPc expressing follicular dendritic cells could serve as a prion "reservoir" during the latency phase, thus playing a key role during the scrapie lymphoinvasion.

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“…How the causative agent is conveyed from peripheral entry sites to its targets within the central nervous system (CNS) is a major issue that remains incompletely elucidated. There is now good evidence that the lymphoreticular system (LRS) and the peripheral nervous system (PNS) may both play a crucial role in this process (8,20,30,31,35,38,44). Spleen and gut lymphoid tissues are early sites of prion accumulation or replication in peripherally infected rodents and naturally infected sheep.…”

mentioning

confidence: 99%

Cultured Peripheral Neuroglial Cells Are Highly Permissive to Sheep Prion Infection

Archer

Bachelin

Andréoletti

et al. 2004

J Virol

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The immunobiology of TSE diseases

Abstract: The role of B lymphocytes in TSE pathogenesis The accumulation of scrapie infectivity in the spleen and subsequent neuroinvasion are significantly impaired in mice deficient in B lymphocytes alone (µMT mice ; Klein et al., 1997)

Cited by 73 publications

References 99 publications

Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms

Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms

Features of follicular dendritic cells in ovine pharyngeal tonsil: An in vivo and in vitro study in the context of scrapie pathogenesis

Cultured Peripheral Neuroglial Cells Are Highly Permissive to Sheep Prion Infection

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