Please use this identifier to cite or link to this item: https://doi.org/10.3389/fimmu.2018.00261
Title: Calcineurin B in CD4+ T Cells prevents autoimmune colitis by negatively regulating the JAK/STAT pathway
Authors: Mencarelli, A 
Vacca, M 
Khameneh, H.J
Acerbi, E
Tay, A
Zolezzi, F
Poidinger, M 
Mortellaro, A 
Keywords: ampicillin
calcineurin
gamma interferon
Hermes antigen
interleukin 12
ionomycin
metronidazole
streptomycin
vancomycin
animal cell
animal experiment
animal model
apoptosis
Article
autoimmune disease
body weight gain
bone marrow cell
CD4+ T lymphocyte
cell activation
cell differentiation
cell infiltration
cell isolation
cell migration
cell proliferation
colitis
controlled study
cytokine production
disease predisposition
enteritis
enzyme linked immunosorbent assay
flow cytometry
gene expression
helper cell
histology
homeostasis
inflammatory bowel disease
intestine flora
JAK-STAT signaling
lamina propria
microarray analysis
mouse
nonhuman
regulatory T lymphocyte
scoring system
Th1 cell
Th17 cell
thymus
Issue Date: 2018
Citation: Mencarelli, A, Vacca, M, Khameneh, H.J, Acerbi, E, Tay, A, Zolezzi, F, Poidinger, M, Mortellaro, A (2018). Calcineurin B in CD4+ T Cells prevents autoimmune colitis by negatively regulating the JAK/STAT pathway. Frontiers in Immunology 9 (FEB) : 261. ScholarBank@NUS Repository. https://doi.org/10.3389/fimmu.2018.00261
Abstract: Calcineurin (Cn) is a protein phosphatase that regulates the activation of the nuclear factor of activated T-cells (NFAT) family of transcription factors, which are key regulators of T-cell development and function. Here, we generated a conditional Cnb1 mouse model in which Cnb1 was specifically deleted in CD4+ T cells (Cnb1CD4 mice) to delineate the role of the Cn-NFAT pathway in immune homeostasis of the intestine. The Cnb1CD4 mice developed severe, spontaneous colitis characterized at the molecular level by an increased T helper-1-cell response but an unaltered regulatory T-cell compartment. Antibiotic treatment ameliorated the intestinal inflammation observed in Cnb1CD4 mice, suggesting that the microbiota contributes to the onset of colitis. CD4+ T cells isolated from Cnb1CD4 mice produced high levels of IFN? due to increased activation of the JAK2/STAT4 pathway induced by IL-12. Our data highlight that Cn signaling in CD4+ T cells is critical for intestinal immune homeostasis in part by inhibiting IL-12 responsiveness of CD4+ T cells. © 2018 Mencarelli, Vacca, Khameneh, Acerbi, Tay, Zolezzi, Poidinger and Mortellaro.
Source Title: Frontiers in Immunology
URI: https://scholarbank.nus.edu.sg/handle/10635/173738
ISSN: 16643224
DOI: 10.3389/fimmu.2018.00261
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