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Responsible editor | Enzyme beauty dendritic cells (dendritic cells, DC) are the bridge connecting the body's innate immunity and adaptive immunity, and are the main antigen presenting cells.
In non-inflammatory conditions, DCs mainly include type 1 conventional dendritic cells (type 1 conventional DC, cDC1), cDC2 and plasmacytoid DC (pDC) [1].
cDC1 is the main DC subgroup that presents foreign antigens to T cells.
Activated T cells can specifically kill tumor cells and infected cells, so they play a key role in anti-tumor and anti-infection [2].
Although cDC1 plays an important role in the immune system, its differentiation and development mechanism is still unclear [3].
Immune cell differentiation is mainly regulated by transcription factors.
DC-SCRIPT is a DC-specific and highly expressed transcription factor [4], which is mainly expressed in cDC and its progenitor cells, but not in pDC, and is highly expressed in cDC1.
But the role of DC-SCRIPT in DC is still unknown.
The impact of DC-SCRIPT on DC differentiation and function is the core issue of this study.
Recently, the team of Professor Steph Nutt and Dr.
Michael Chopin from the WEHI Institute of the University of Melbourne published a research paper titled Type 1 conventional dendritic cell fate and function are controlled by DC-SCRIPT online in Science Immunology.
And was selected as the cover of the magazine.
The study found that the loss of DC-SCRIPT would seriously affect the development and function of cDC1, and its mechanism was deeply explored at the transcriptome level and genome level.
The research group successfully constructed DC-SCRIPT fluorescent reporter mice, and found that DC-SCRIPT expressed highly specificity in cDC1 in the lymph nodes, spleen, liver, lung, small intestine and other organs of mice.
Flow cytometric analysis of hematopoietic stem cells in bone marrow was performed.
It was found that DC-SCRIPT began to be expressed in pre-cDC1, the progenitor cell of cDC1, and was a specific marker molecule for cDC1 lineage differentiation.
In addition, the research team found through the construction of DC-SCTRIPT knockout mice that the lack of DC-SCRIPT can impair the differentiation of cDC1, but does not hinder the differentiation of cDC2.
The author analyzed the DC-SCRIPT knockout cDC1 at the transcriptome level and found that its cDC1 specific marker gene expression was down-regulated, while the cDC2 marker gene was up-regulated, indicating that DC-SCRIPT has an important regulatory effect on the expression of cDC1 specific genes.
The high-level expression of IRF8 is critical to the differentiation of cDC1.
DC-SCRIPT knockout cDC1 cannot maintain the high expression of IRF8.
ChIPseq results show that DC-SCRIPT will bind to the +32kb enhancer region of IRF8 to promote the high expression of IRF8.
Therefore, DC-SCRIPT may regulate the differentiation of cDC1 by promoting the expression of IRF8.
Functionally, the absence of DC-SCRIPT will damage the endocytosis of cDC1, which will hinder the cross-presentation of antigens and affect the activation of T cells.
In addition, DC-SCRIPT directly regulates the expression of IL-12 and plays an important role in the fight against Toxoplasma gondii infection.
Dr.
Zhang Shengbo from the WEHI Institute of the University of Melbourne, Australia is the first author of this article; Professor Stephen Nutt and Dr.
Michael Chopin, academicians of the Australian Academy of Sciences, are the co-corresponding authors of this article; this research is strongly supported by Professor Zhan Yifan of Huaaotai Biotechnology (Shanghai).Original link: http://immunology.
sciencemag.
org/lookup/doi/10.
1126/sciimmunol.
abf4432 Platemaker: 11 References 1.
GT Belz, SL Nutt, Transcriptional programming of the dendritic cell network.
Nature reviews.
Immunology 12 , 101-113 (2012).
2.
ST Ferris et al.
, cDC1 prime and are licensed by CD4(+) T cells to induce anti-tumour immunity.
Nature 584, 624-629 (2020).
3.
SL Nutt, M.
Chopin, Transcriptional Networks Driving Dendritic Cell Differentiation and Function.
Immunity 52, 942-956 (2020).
4.
M.
Chopin et al.
, Transcription Factor PU.
1 Promotes Conventional Dendritic Cell Identity and Function via Induction of Transcriptional Regulator DC -SCRIPT.
Immunity 50, 77-90 e75 (2019).
Reprinting instructions [Non-original articles] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting is prohibited without permission.
The author has all legal rights, and offenders must be investigated.
In non-inflammatory conditions, DCs mainly include type 1 conventional dendritic cells (type 1 conventional DC, cDC1), cDC2 and plasmacytoid DC (pDC) [1].
cDC1 is the main DC subgroup that presents foreign antigens to T cells.
Activated T cells can specifically kill tumor cells and infected cells, so they play a key role in anti-tumor and anti-infection [2].
Although cDC1 plays an important role in the immune system, its differentiation and development mechanism is still unclear [3].
Immune cell differentiation is mainly regulated by transcription factors.
DC-SCRIPT is a DC-specific and highly expressed transcription factor [4], which is mainly expressed in cDC and its progenitor cells, but not in pDC, and is highly expressed in cDC1.
But the role of DC-SCRIPT in DC is still unknown.
The impact of DC-SCRIPT on DC differentiation and function is the core issue of this study.
Recently, the team of Professor Steph Nutt and Dr.
Michael Chopin from the WEHI Institute of the University of Melbourne published a research paper titled Type 1 conventional dendritic cell fate and function are controlled by DC-SCRIPT online in Science Immunology.
And was selected as the cover of the magazine.
The study found that the loss of DC-SCRIPT would seriously affect the development and function of cDC1, and its mechanism was deeply explored at the transcriptome level and genome level.
The research group successfully constructed DC-SCRIPT fluorescent reporter mice, and found that DC-SCRIPT expressed highly specificity in cDC1 in the lymph nodes, spleen, liver, lung, small intestine and other organs of mice.
Flow cytometric analysis of hematopoietic stem cells in bone marrow was performed.
It was found that DC-SCRIPT began to be expressed in pre-cDC1, the progenitor cell of cDC1, and was a specific marker molecule for cDC1 lineage differentiation.
In addition, the research team found through the construction of DC-SCTRIPT knockout mice that the lack of DC-SCRIPT can impair the differentiation of cDC1, but does not hinder the differentiation of cDC2.
The author analyzed the DC-SCRIPT knockout cDC1 at the transcriptome level and found that its cDC1 specific marker gene expression was down-regulated, while the cDC2 marker gene was up-regulated, indicating that DC-SCRIPT has an important regulatory effect on the expression of cDC1 specific genes.
The high-level expression of IRF8 is critical to the differentiation of cDC1.
DC-SCRIPT knockout cDC1 cannot maintain the high expression of IRF8.
ChIPseq results show that DC-SCRIPT will bind to the +32kb enhancer region of IRF8 to promote the high expression of IRF8.
Therefore, DC-SCRIPT may regulate the differentiation of cDC1 by promoting the expression of IRF8.
Functionally, the absence of DC-SCRIPT will damage the endocytosis of cDC1, which will hinder the cross-presentation of antigens and affect the activation of T cells.
In addition, DC-SCRIPT directly regulates the expression of IL-12 and plays an important role in the fight against Toxoplasma gondii infection.
Dr.
Zhang Shengbo from the WEHI Institute of the University of Melbourne, Australia is the first author of this article; Professor Stephen Nutt and Dr.
Michael Chopin, academicians of the Australian Academy of Sciences, are the co-corresponding authors of this article; this research is strongly supported by Professor Zhan Yifan of Huaaotai Biotechnology (Shanghai).Original link: http://immunology.
sciencemag.
org/lookup/doi/10.
1126/sciimmunol.
abf4432 Platemaker: 11 References 1.
GT Belz, SL Nutt, Transcriptional programming of the dendritic cell network.
Nature reviews.
Immunology 12 , 101-113 (2012).
2.
ST Ferris et al.
, cDC1 prime and are licensed by CD4(+) T cells to induce anti-tumour immunity.
Nature 584, 624-629 (2020).
3.
SL Nutt, M.
Chopin, Transcriptional Networks Driving Dendritic Cell Differentiation and Function.
Immunity 52, 942-956 (2020).
4.
M.
Chopin et al.
, Transcription Factor PU.
1 Promotes Conventional Dendritic Cell Identity and Function via Induction of Transcriptional Regulator DC -SCRIPT.
Immunity 50, 77-90 e75 (2019).
Reprinting instructions [Non-original articles] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting is prohibited without permission.
The author has all legal rights, and offenders must be investigated.
