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Regulation and dysregulation of innate immunity by NFAT signaling downstream of PRRs.

06:00 EDT 19th June 2012 | BioPortfolio

Summary of "Regulation and dysregulation of innate immunity by NFAT signaling downstream of PRRs."

Innate immunity is the most ancient form of response to pathogens and it relies on evolutionary conserved signaling pathways, i.e. those involving the NF-κB pathway. Nevertheless, increasing evidence suggests that factors that have appeared more recently in evolution, such as the Nuclear Factor of Activated T cell transcription factor family (NFATc), also contribute to innate immune-response regulation in vertebrates. Exposure to inflammatory stimuli induces the activation of NFATc factors in innate immune cells, including conventional dendritic cells (DCs), granulocytes, mast cells and, under pathological circumstances, also macrophages. While the evolutionary conserved functions of innate immunity, such as direct microbial killing and interferon (IFN) production, are expected to be NFATc independent, other aspects of innate immunity, including collaboration with adaptive immunity and mechanisms to limit the tissue damage generated by the inflammatory process, are presumably controlled by NFATc members in collaboration with other transcription factors. In this article, we discuss the recent advances regarding the role of the NFATc signaling pathway in regulating DC, neutrophil and macrophage responses to specific inflammatory stimuli, including lipopolysaccharide (LPS) and β-glucan-bearing microorganisms. We also discuss how NFATc signaling influences the interactions of myeloid cells with lymphocytes.

Affiliation

Department of Biotechnology and Biosciences, University of Milano-Bicocca, Piazza della Scienza 2, 20126, Milan, Italy.

Journal Details

This article was published in the following journal.

Name: European journal of immunology
ISSN: 1521-4141
Pages:

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