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Transcriptomic landscape for lymphocyte count variation in poly I:C‐induced porcine peripheral blood
- Wang, H., Hou, Y., Guo, J., Chen, H., Liu, X., Wu, Z., Zhao, S., Zhu, M.
- Animal genetics 2016 v.47 no.1 pp. 49-61
- adaptive immunity, apoptosis, blood, chemokines, cytotoxicity, gene expression, gene expression regulation, genes, innate immunity, lymphocyte count, signal transduction, swine, transcriptome, transcriptomics
- Lymphocyte count is an important phenotypic metric that has been reported to be related to the individual antiviral capacity of pigs and other mammals. To date, aside from information regarding several genes and pathways, little is known about the mechanism by which gene expression affects variation in lymphocyte count. In this work, we investigated the lymphocyte count variation after poly I:C stimulation and compared the transcriptomes of pigs with large and small differences of lymphocyte counts before and after poly I:C stimulation. Pigs with large and small differences of lymphocyte counts were designated as extreme response (ER) and moderate response (MR) pigs respectively. Lymphocyte counts in all animals were observed to decline after poly I:C stimulation. Transcriptomic analysis identified 1121 transcripts (981 differentially expressed genes) in MR pigs and 1045 transcripts (904 differentially expressed genes) in ER pigs. We found that the majority of the differentially expressed genes were involved in both innate and adaptive immune responses. However, the innate immune response of ER pigs was more rapid than that of MR pigs. Results indicated that the activation of signaling pathways associated with cell death, cytotoxicity and apoptosis may contribute to the poly I:C‐induced decrease of lymphocyte counts in the periphery. Moreover, the differential expression patterns of chemokines and FAS either totally or partially provided an interpretation for the different degrees of decrease in the lymphocyte counts between MR and ER pigs. Overall, our study will provide further understanding of the molecular basis for the antiviral capacity of pigs and other mammals.