The <i>Ccl17</i> gene encoding TARC is synergistically transactivated by PU.1 and IRF4 driven by the mammalian common promoter in dendritic cells

Ito, Naoto; Sakata, Fumihiko; Hachisu, Mitsugu; Nagata, Kazuki; Ito, Tomoka; Nomura, Kurumi; Nagaoka, Masanori; Inaba, Keito; Hara, Mutsuko; Nakano, Nobuhiro; Nakajima, Tasuku; Yashiro, Takashi; Nishiyama, Chiharu

doi:10.1111/all.15184

Cited by 8 publications

(9 citation statements)

References 6 publications

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“…7d ). The transcript level of Ccr7 was also markedly decreased in PU.1 KD DCs, which was likely a result of the decreased expression of the Irf4 , which is under the control of PU.1 18 , and to the KD of PU.1 itself, which transactivates the Ccr7 gene in DCs 19 .…”

Section: Resultsmentioning

confidence: 97%

NR4A3 deficiency ameliorates contact hypersensitivity and exacerbates psoriasis by regulating gene expression in dendritic cells

Katagiri,

Ito,

Nagata

et al. 2024

Preprint

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NR4A3 is a transcription factor that belongs to the nuclear receptor superfamily. To reveal the roles of NR4A3 in skin diseases, we constructed contact hypersensitivity (CHS)- and imiquimod-induced psoriasis models inNr4a3-/-mice. In the CHS inducedNr4a3-/-mice, ear swelling was significantly reduced, accompanied by suppressed migration of dendritic cells (DCs), in which CCR7 expression was reduced. In contrast, ear swelling in psoriasis modelNr4a3-/-mice was enhanced. The expression levels of inflammatory cytokines in psoriasis skin lesions and in TLR7-ligand-stimulated DCs were increased by NR4A3 deficiency. Subcutaneous (s.c.) injection of hapten-treatedNr4a3+/+DCs induced ear swelling inNr4a3-/-mice, and s.c. injection of TLR7-ligand-stimulatedNr4a3-/-DCs caused significant ear swelling. Compared withNr4a3+/+DCs,Nr4a3-/-DCs expressed lower levels of CCR7 and IRF4, and higher levels of TLR7, IRF7, IFN-β, and PU.1. Taken together, NR4A3 deficiency ameliorates CHS and exacerbates psoriasis by regulating the expression of CCR7, TLR7, and related transcription factors in DCs.

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Section: Resultsmentioning

confidence: 97%

NR4A3 deficiency ameliorates contact hypersensitivity and exacerbates psoriasis by regulating gene expression in dendritic cells

Katagiri,

Ito,

Nagata

et al. 2024

Preprint

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“…Total RNA was extracted from BMDCs using the ReliaPrep RNA Cell Miniprep System (#Z6012, Promega, Madison, USA) and from the skin using ISOGEN (#311-02501, Nippongene, Tokyo, Japan). Synthesis of cDNA, and quantitative PCR were performed as previously described ( 10 ). The nucleotide sequences of the primer sets are listed in Supplementary Table 1 .…”

Section: Methodsmentioning

confidence: 99%

A rose flavor compound activating the NRF2 pathway in dendritic cells ameliorates contact hypersensitivity in mice

Kodama

Okada²,

Hachisu³

et al. 2023

Front. Nutr.

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Dendritic cells (DCs), which are typical antigen-presenting cells, localize to various sites in the body, particularly the front line of infection as sentinels, and are involved in innate and adaptive immune responses. Although the functions of DCs, such as pathogen-induced cytokine production and antigen-specific T cell activation, are important for host defenses against infection and tumorigenesis, the hyper- and/or extended activation of DCs leads to inflammatory and autoimmune diseases. In the present study, β-damascone, a major ingredient of rose fragrance, was selected from an aroma library as a candidate compound that suppresses antigen-induced immune responses. β-Damascone inhibited the functions of DCs, including the antigen-dependent proliferation of T cells, DC-induced Th1 development, and the TLR ligand-induced production of inflammatory cytokines by DCs. The β-damascone treatment also increased the protein level of the transcription factor NF-E2-related factor 2 (NRF2), which plays key roles in antioxidant responses, and the transcription of Hmox1 and Nqo1, target genes of NRF2, in DCs. Nrf2–/– DCs induced Th1-development and produced large amount of IL-12p40 even in the presence of β-damascone, whereas these functions by Nrf2+/– DCs were inhibited by β-damascone under the same conditions. The intake of β-damascone suppressed ear swelling in contact hypersensitivity (CHS) model mice, but not in CHS-induced Nrf2–/– mice. Collectively, the present results indicate the potential of the rose aroma compound β-damascone, which suppresses DC-mediated immune responses by activating the NRF2 pathway in DCs, for the prevention and/or attenuation of immune-mediated diseases.

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“…The extraction of total RNA, synthesis of cDNA, and quantitative PCR were performed as previously described (13).…”

Section: Methodsmentioning

confidence: 99%

The gut lactic acid bacteria metabolite, 10-oxo-cis-6,trans-11-octadecadienoic acid, suppresses inflammatory bowel disease in mice by modulating the NRF2 pathway and GPCR-signaling

Nagata

Ito

Noguchi

et al. 2023

Preprint

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Various gut bacteria, including Lactobacillus plantarum, possess several enzymes that produce hydroxy fatty acids (FAs), oxo FAs, conjugated FAs, and partially saturated FAs from polyunsaturated FAs as secondary metabolites. Among these derivatives, we identified 10-oxo-cis-6,trans-11-octadecadienoic acid (gammaKetoC), a gamma-linolenic acid-derived enon FA, as the most effective immunomodulator, which inhibited the antigen-induced immunoactivation and the LPS-induced production of inflammatory cytokines. The treatment with gammaKetoC markedly increased the protein level of NRF2, a master transcription factor for antioxidant responses, and the mRNA level of Hmox1, a target gene of NRF2, in bone marrow-derived dendritic cells (BMDCs). Although gammaKetoC significantly suppressed the LPS-induced activation of control BMDCs, particularly the secretion of IL-12/23p40, the suppressive effects of gammaKetoC were reduced in Nrf2-/- BMDCs. GW9508, an agonist of GPR40/GPR120, inhibited the release of cytokines from LPS-stimulated BMDCs without activating the NRF2 pathway. We evaluated the role of NRF2 in the anti-inflammatory effects of gammaKetoC in a dextran sodium sulfate-induced colitis model. The oral administration of gammaKetoC significantly reduced body weight loss, improved stool scores, and attenuated atrophy of the colon, in wild-type C57BL/6J and Nrf2+/- (C57BL/6N) mice with colitis. In contrast, the pathology of colitis was deteriorated in Nrf2-/- mice even with the administration of gammaKetoC. Collectively, the present results demonstrated the involvement of the NRF2 pathway in gammaKetoC-mediated anti-inflammatory responses.

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The Ccl17 gene encoding TARC is synergistically transactivated by PU.1 and IRF4 driven by the mammalian common promoter in dendritic cells

Abstract: A CCL1/CCR8dependent feed-forward mechanism drives ILC2 functions in type 2-mediated inflammation.

Cited by 8 publications

References 6 publications

NR4A3 deficiency ameliorates contact hypersensitivity and exacerbates psoriasis by regulating gene expression in dendritic cells

NR4A3 deficiency ameliorates contact hypersensitivity and exacerbates psoriasis by regulating gene expression in dendritic cells

A rose flavor compound activating the NRF2 pathway in dendritic cells ameliorates contact hypersensitivity in mice

The gut lactic acid bacteria metabolite, 10-oxo-cis-6,trans-11-octadecadienoic acid, suppresses inflammatory bowel disease in mice by modulating the NRF2 pathway and GPCR-signaling

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