| dc.creator |
Shack, Leslie |
|
| dc.creator |
Buza, Joram |
|
| dc.creator |
Burgess, Shane |
|
| dc.date |
2019-10-07T10:29:56Z |
|
| dc.date |
2019-10-07T10:29:56Z |
|
| dc.date |
2008-02-07 |
|
| dc.date.accessioned |
2022-10-25T09:20:48Z |
|
| dc.date.available |
2022-10-25T09:20:48Z |
|
| dc.identifier |
https://doi 10.1007/s00262-008-0460-2 |
|
| dc.identifier |
http://dspace.nm-aist.ac.tz/handle/123456789/456 |
|
| dc.identifier.uri |
http://hdl.handle.net/123456789/95250 |
|
| dc.description |
Research Article published by Springer-Verlag |
|
| dc.description |
Introduction Marek’s disease (MD), a herpesvirus-induced
lymphoma of chickens is a unique natural model of CD30-
overexpressing (CD30hi) lymphoma. We have previously
proposed that the CD30hi neoplastically transformed CD4+ T
cells in MD lymphomas have a phenotype antagonistic to
cell mediated immunity. Here were test the hypothesis that
the CD30hi neoplastically transformed MD lymphoma cells
have a phenotype more closely resembling T-helper (Th)-2
or regulatory T (T-reg) cells.
Materials and methods We separated ex vivo-derived
CD30hi, from the CD30lo/¡ (non-transformed), MD lymphoma
cells and then quantiWed the relative amounts of
mRNA and proteins for cytokines and other genes that
deWne CD4+ Th-1, Th-2 or T-reg phenotypes.
Results and discussion Gene Ontology-based modeling
of our data shows that the CD30hi MD lymphoma cells
having a phenotype more similar to T-reg. Sequences that
could be bound by the MD virus putative oncoprotein Meq
in each of these genes’ promoters suggests that the MD herpesvirus may play a direct role in maintaining this
T-reg-like phenotype. |
|
| dc.format |
application/pdf |
|
| dc.language |
en |
|
| dc.publisher |
Springer-Verlag |
|
| dc.subject |
Regulatory T cell |
|
| dc.subject |
Gene Ontology |
|
| dc.subject |
Systems biology |
|
| dc.subject |
Animal model |
|
| dc.title |
The neoplastically transformed (CD30hi) Marek’s disease lymphoma cell phenotype most closely resembles T-regulatory cells |
|
| dc.type |
Article |
|