Reppert S, Zinser E, Holzinger C, Sandrock L, Koch S, Finotto S (2015)
Publication Type: Journal article
Publication year: 2015
Publisher: Wiley-VCH Verlag
Book Volume: 45
Pages Range: 1426-40
Journal Issue: 5
NFATc1 is a member of the nuclear factor of activated T cells (NFAT) family of transcription factors. NFAT is activated upon T-cell receptor activation followed by intracytoplasmatic calcium influx where calmodulin, a calcium sensor protein, activates the phosphatase calcineurin that dephosphorylates NFAT proteins and results in NFAT nuclear import. Here, we show the analysis of conditional NFATc1-deficient mice bearing a deletion of NFATc1 in CD4(+) and CD8(+) T cells. NFATc1-deficient CD4(+) T cells polarized under Th17 conditions express reduced levels of the Th17-associated transcription factor ROR?T (where ROR is RAR-related orphan receptor) as well as the Th17-associated cytokines IL-17A, IL-17F, IL-21, and IL-10. In the murine model of experimental EAE, we found a strong reduction of the disease outcome in conditional NFATc1-deficient mice, as compared with control littermates. This was accompanied by a diminished inflammation in the brain and spinal cord and reduced IL-17A and IFN-? expression by antigen-specific spleen, spinal cord, and brain cells. Altogether, these results reveal an important role of NFATc1 in inducing Th17-cell responses and IFN-?, both being relevant for the EAE development.
APA:
Reppert, S., Zinser, E., Holzinger, C., Sandrock, L., Koch, S., & Finotto, S. (2015). NFATc1 deficiency in T cells protects mice from experimental autoimmune encephalomyelitis. European Journal of Immunology, 45(5), 1426-40. https://doi.org/10.1002/eji.201445150
MLA:
Reppert, Sarah, et al. "NFATc1 deficiency in T cells protects mice from experimental autoimmune encephalomyelitis." European Journal of Immunology 45.5 (2015): 1426-40.
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