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Open AccessHighly AccessResearch article

Genome-wide gene expression profiling of human mast cells stimulated by IgE or FcεRI-aggregation reveals a complex network of genes involved in inflammatory responses

Manikandan Jayapal1 email, Hwee Kee Tay1 email, Renji Reghunathan1 email, Liang Zhi1 email, Kah Kiong Chow2 email, Mary Rauff3 email and Alirio J Melendez1 email

1Department of Physiology, National University of Singapore, Singapore

2Department of Obstetrics & Gynecology, Gleneagles Medical Centre, Singapore

3Department of Obstetrics & Gynecology, National University of Singapore, Singapore

author email corresponding author email

BMC Genomics 2006, 7:210doi:10.1186/1471-2164-7-210

Published: 16 August 2006

Abstract

Background

Mast cells are well established effectors of IgE-triggered allergic reactions and immune responses to parasitic infections. Recent studies indicate that mast cells may play roles in adaptive and innate immunity, suggesting an innovative view of the regulation of immune responses. Here, we profiled the transcriptome of human mast cells sensitized with IgE alone, or stimulated by FcεRI aggregation.

Results

Our data show that among 8,793 genes examined, 559 genes are differentially regulated in stimulated mast cells when compared with resting/unstimulated mast cells. The major functional categories of upregulated genes include cytokines, chemokines, and other genes involved in innate and adaptive immune-responses. We observed the increased expression of over 63 gene-transcripts following IgE-sensitization alone. Our data was validated using Real-Time-PCR; ELISA and western blot. We confirmed that IgE alone does not trigger mast cell-immediate responses, such as calcium signals, degranulation or protein-phosphorylation.

Conclusion

This report represents a substantial advance in our understanding of the genome wide effects triggered by "passive sensitization" or active stimulation of human mast cells, supporting mast cells' potential involvement in a wide range of inflammatory responses.


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