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Genotype-Dependent Tumor Regression in Marek’s Disease Mediated at the Level of Tumor Immunity

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dc.contributor.author Kumar, Shyamesh
dc.contributor.author Buza, Joram J.
dc.contributor.author Burgess, Shane C.
dc.date.accessioned 2019-10-08T05:34:51Z
dc.date.available 2019-10-08T05:34:51Z
dc.date.issued 2008-03-18
dc.identifier.uri DOI 10.1007/s12307-008-0018-z
dc.identifier.uri http://dspace.nm-aist.ac.tz/handle/123456789/462
dc.description Research Article published by Springer en_US
dc.description.abstract Marek’s disease (MD) of chickens is a unique natural model of Hodgkin’s and Non Hodgkin’s lymphomas in which the neoplastically-transformed cells over-express CD30 (CD30hi) antigen. All chicken genotypes can be infected with MD virus and develop microscopic lymphomas. From 21 days post infection (dpi) microscopic lymphomas regress in resistant chickens but, in contrast, they progress to gross lymphomas in susceptible chickens. Here we test our hypothesis that in resistant chickens at 21 dpi the tissue microenvironment is pro T-helper (Th)-1 and compatible with cytotoxic T lymphocyte (CTL) immunity but in susceptible lines it is pro Th-2 or pro T-regulatory (T-reg) and antagonistic to CTL immunity. We used the B2, non-MHC-associated, MD resistance/susceptibility system (line [L]61/line [L]72) and quantified the levels of key mRNAs that can be used to define Th-1 (IL-2, IL-12, IL-18, IFNγ), Th-2 (IL-4, IL-10) and T-reg (TGFβ, GPR-83, CTLA-4, SMAD-7) lymphocyte phenotypes. We measured gene expression in both whole tissues (represents tissue microenvironment and tumor microenvironment) and in the lymphoma lesions (tumor microenvironment) themselves. Gene ontology-based modeling of our results shows that the dominant phenotype in whole tissue as well as in microscopic lymphoma lesions, is pro T-reg in both L61 and L72 but a minor pro Th-1 and anti Th-2 tissue microenvironment exists in L61 whereas there is an anti Th-1 and pro Th-2 tissue microenvironment in L72. The tumor microenvironment per se is pro T-reg, anti Th-1 and pro Th-2 in both L61 and L72. Together our data suggests that the neoplastic transformation is essentially the same in both L61 and L72 and that resistance/susceptibility is en_US
dc.language.iso en en_US
dc.publisher Springer en_US
dc.subject Gene ontology en_US
dc.subject Animal model en_US
dc.subject Regulatory Tcell en_US
dc.subject Microenvironment en_US
dc.title Genotype-Dependent Tumor Regression in Marek’s Disease Mediated at the Level of Tumor Immunity en_US
dc.type Article en_US


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