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Development of gene expression signatures on immunity for bursal peptide BPP-II

ABSTRACT: To further elucidate the mechanism of BPP-II on immunity on the broad molecular level, we have employed whole genome microarray expression profiling as a discovery platform to examine gene expression patterns during BPP-II treatment in a mouse derived hybridoma culture system. Hybridoma cell was treated ex vivo, and robust normalization of the data identified 2478 differentially expressed probe sets exhibiting minimum 1.5-fold changes that distinguished between BPP-II and control samples. Various pathwayswere significantly impacted by BPP-II treatment, and gene Ontology annotations show changes in the expression of molecules involved in immune and immunocyte related cellular processes. Expression of 8 genes (MS4A2，CD86，CD80， Fas，CDKN2A，CBLC, FGF21 and Fyn) from this signature was quantified in the RNA samples by QRT-PCR, confirming low variability between the predicted response patterns.

ORGANISM(S): Mus musculus

PROVIDER: GSE28696 | GEO | 2011/04/19

SECONDARY ACCESSION(S): PRJNA138907

REPOSITORIES: GEO

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Project description:Canine cutaneous histiocytoma (CCH) is a tumor originating from dermal Langerhans cells, especially affecting young dogs. The common spontaneous regression of CCH makes it an interesting model in comparative oncology research. Previous studies have indicated that anti-tumor immune responses may be involved but details remain speculative to date. Here, we asked which specific immuno-oncological dynamics underlie spontaneous regression of CCH on mRNA and protein levels. QuantSeq 3' mRNA sequencing with functional overrepresentation analysis and an nCounter RNA hybridization assay were employed on 21 formalin-fixed, paraffin-embedded CCH samples representing three different tumor stages. Nine additional samples were subjected to matrix-assisted laser desorption ionization mass spectrometry imaging (MALDI-MSI). Surprisingly, only minor stage-specific differences were found. When we investigated expression of B7 family ligands and CD28 family receptors holding co-stimulatory and -inhibitory functions respectively, we found higher abundance of CD80, CD86 and CD28, which trigger activation of lymphocyte-mediated immune responses. CD80 and CD86 expressing cells were further quantified by in situ hybridization and compared with data from three cases of canine histiocytic sarcoma (HS), a malignant tumor variant originating from antigen presenting cells. A stage-specific increase of CD80 expression was recorded in CCH from the tumor bottom to the top, while CD86 was continuously and homogenously expressed at high levels. Expression of CD80 in CCH was similar to that in HS (73.3 ± 37.4% versus 62.1 ± 46.4% positive cells), while CD86 was significantly higher expressed in CCH (94.7 ± 10.3%) when compared to HS (57.6 ± 11.0%). Our data suggest that major immuno-oncological pathways are seemingly not regulated during regression of CCH on the mRNA or protein levels as detectable by the methods used. We speculate that key signals leading to tumor regression may occur at an interactome level or at an earlier time point than examined here. Our data further supports a role of immune stimulatory B7 family ligands and CD28 family receptors in CCH regression.

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Development of gene expression signatures on immunity for bursal peptide BPP-II

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