Unknown,Transcriptomics,Genomics,Proteomics

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Murine CD8 T cell gene expression in reponse to type I interferon

ABSTRACT: To investigate type I interferon regulated genes in CD8+ T cells, we used microarray analyses after stimulation of primary murine T cell cultures. Negatively sorted T cells from naive C57Bl/6 mice were incubated with PBS or anti-CD3 in presence or absence of type I interferon (IFN-4a, 500U/mL). After 6h total RNA was extracted from the primary T cell cultures and microarrays were performed after RNA quality control. Among significantly regulated genes, we identified NK cell receptor ligands to be affected by exposure to type I interferon. 10^6 negatively sorted CD8+ T cells were stimulated with anti-CD3 antibody in the presence or absence of IFN-4a. Additionally, CD8+ cells were mock treated with PBS in the presence or absence of IFN-4a. After 6h, total RNA was extracted from cell suspensions and microarray analyses were performed. All experiments were carried out in triplicates.

ORGANISM(S): Mus musculus

SUBMITTER: Rene Deenen

PROVIDER: E-GEOD-57421 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Comparison of two Chlamydia-specific CD4 T cells that are dependent on iNOS to terminate Chlamydia replication in epithelial cells to two Chlamydia-specific CD4 T cells that are iNOS-independent: Chlamydia trachomatis urogenital serovars replicate predominately in epithelial cells lining the reproductive tract. This tissue tropism poses a unique challenge for the host immune system and vaccine development. Studies utilizing the Chlamydia muridarum mouse model have shown that CD4 T cells are critical and sufficient to clear primary genital tract infections. In vitro studies have shown that CD4 T cells terminate the infection in epithelial cells by up regulating epithelial iNOS transcription and nitric oxide production via IFN-gamma and T cell-epithelial cell interactions mediated by LFA-1-ICAM-1. This mechanism however is not critical as iNOS-deficient mice clear infections normally, and IFN-gamma deficient mice clear 99.9% of the infection with near normal kinetics. We recently showed that a subset of Chlamydia-specific CD4 T cell clones were able to terminate replication in epithelial cells using a mechanism that was independent of iNOS and IFN-gamma. That mechanism did not require physical lysis of infected cells, but instead required T cell degranulation. In this study we advanced that work using gene expression microarrays to compare CD4 T cell clones that are able to terminate epithelial replication via an iNOS-independent mechanism to iNOS-dependent CD4 T cell clones. Micro array experiments showed that Plac8 was differentially expressed by the T cell clones having the iNOS-independent mechanism. Plac8-deficient mice had significantly delayed clearance of C. muridarum genital tract infections, and that the large majority of Plac8-deficient mice treated with the iNOS-inhibitor N-monomethyl-L-arginine (MLA) were unable to resolve a C. muridarum genital tract infection over 8 weeks. These results demonstrate that there are two independent and redundant T cell mechanisms for clearing C. muridarum genital tract infections; one mechanism dependent on iNOS, the other mechanism dependent on Plac8. While T cells subsets have been defined by cytokine profiles, there are important subdivisions by effector functions, in this case CD4Plac8. Gene expression study using 4 experimental groups with 4 replicates each.

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Murine CD8 T cell gene expression in reponse to type I interferon

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