Dermal IRF4+ dendritic cells and monocytes license CD4+ T helper cells to distinct cytokine profiles

Antigen (Ag)-presenting cells (APC) instruct CD4+ helper T (Th) cell responses, but it is unclear whether different APC subsets contribute uniquely in determining Th differentiation in pathogen-specific settings. Here, we use skin-relevant, fluorescently-labeled bacterial, helminth or fungal pathoge...

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Published inNature communications Vol. 11; no. 1; p. 5637
Main Authors Hilligan, Kerry L., Tang, Shiau-Choot, Hyde, Evelyn J., Roussel, Elsa, Mayer, Johannes U., Yang, Jianping, Wakelin, Kirsty A., Schmidt, Alfonso J., Connor, Lisa M., Sher, Alan, MacDonald, Andrew S., Ronchese, Franca
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 06.11.2020
Nature Publishing Group
Nature Portfolio
Subjects
13
13/21
13/31
631/250/1619/554/1898
631/250/21/1293
631/250/2499
631/250/2504/133
64/110
64/60
Animals
Antigen-presenting cells
Antigen-Presenting Cells - immunology
Antigens
CD4 antigen
Cell Differentiation
Cell migration
Chemokines
Cytokines
Dendritic cells
Dendritic Cells - immunology
Dendritic structure
Depletion
Differentiation (biology)
Female
Fungi
Helper cells
Humanities and Social Sciences
Inoculation
Interferon regulatory factor 4
Interferon Regulatory Factors - genetics
Interferon Regulatory Factors - immunology
Interferon-gamma - genetics
Interferon-gamma - immunology
Interleukin 12
Interleukin 4
Interleukin-17 - genetics
Interleukin-17 - immunology
Interleukin-4 - genetics
Interleukin-4 - immunology
Lymph nodes
Lymphocyte Activation
Lymphocytes T
Male
Mice
Mice, Inbred C57BL
Monocytes
Monocytes - cytology
Monocytes - immunology
multidisciplinary
Pathogens
Science
Science (multidisciplinary)
Skin
Skin - immunology
T-Lymphocytes, Helper-Inducer - cytology
T-Lymphocytes, Helper-Inducer - immunology
Transcription
γ-Interferon
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Abstract Antigen (Ag)-presenting cells (APC) instruct CD4+ helper T (Th) cell responses, but it is unclear whether different APC subsets contribute uniquely in determining Th differentiation in pathogen-specific settings. Here, we use skin-relevant, fluorescently-labeled bacterial, helminth or fungal pathogens to track and characterize the APC populations that drive Th responses in vivo. All pathogens are taken up by a population of IRF4+ dermal migratory dendritic cells (migDC2) that similarly upregulate surface co-stimulatory molecules but express pathogen-specific cytokine and chemokine transcripts. Depletion of migDC2 reduces the amount of Ag in lymph node and the development of IFNγ, IL-4 and IL-17A responses without gain of other cytokine responses. Ag+ monocytes are an essential source of IL-12 for both innate and adaptive IFNγ production, and inhibit follicular Th cell development. Our results thus suggest that Th cell differentiation does not require specialized APC subsets, but is driven by inducible and pathogen-specific transcriptional programs in Ag+ migDC2 and monocytes. Antigen presenting cells induce CD4+ T helper (Th) differentiation upon pathogen encounters. Here the authors use fluorescently-labeled bacteria, helminth and fungi to track and describe the functions of IRF4+ migratory type 2 dendritic cells and monocytes in the specific induction of Th1, Th2 or Th17 responses following skin inoculation.
AbstractList Antigen (Ag)-presenting cells (APC) instruct CD4+ helper T (Th) cell responses, but it is unclear whether different APC subsets contribute uniquely in determining Th differentiation in pathogen-specific settings. Here, we use skin-relevant, fluorescently-labeled bacterial, helminth or fungal pathogens to track and characterize the APC populations that drive Th responses in vivo. All pathogens are taken up by a population of IRF4+ dermal migratory dendritic cells (migDC2) that similarly upregulate surface co-stimulatory molecules but express pathogen-specific cytokine and chemokine transcripts. Depletion of migDC2 reduces the amount of Ag in lymph node and the development of IFNγ, IL-4 and IL-17A responses without gain of other cytokine responses. Ag+ monocytes are an essential source of IL-12 for both innate and adaptive IFNγ production, and inhibit follicular Th cell development. Our results thus suggest that Th cell differentiation does not require specialized APC subsets, but is driven by inducible and pathogen-specific transcriptional programs in Ag+ migDC2 and monocytes. Antigen presenting cells induce CD4+ T helper (Th) differentiation upon pathogen encounters. Here the authors use fluorescently-labeled bacteria, helminth and fungi to track and describe the functions of IRF4+ migratory type 2 dendritic cells and monocytes in the specific induction of Th1, Th2 or Th17 responses following skin inoculation.
Antigen (Ag)-presenting cells (APC) instruct CD4+ helper T (Th) cell responses, but it is unclear whether different APC subsets contribute uniquely in determining Th differentiation in pathogen-specific settings. Here, we use skin-relevant, fluorescently-labeled bacterial, helminth or fungal pathogens to track and characterize the APC populations that drive Th responses in vivo. All pathogens are taken up by a population of IRF4+ dermal migratory dendritic cells (migDC2) that similarly upregulate surface co-stimulatory molecules but express pathogen-specific cytokine and chemokine transcripts. Depletion of migDC2 reduces the amount of Ag in lymph node and the development of IFNγ, IL-4 and IL-17A responses without gain of other cytokine responses. Ag+ monocytes are an essential source of IL-12 for both innate and adaptive IFNγ production, and inhibit follicular Th cell development. Our results thus suggest that Th cell differentiation does not require specialized APC subsets, but is driven by inducible and pathogen-specific transcriptional programs in Ag+ migDC2 and monocytes.
Antigen presenting cells induce CD4+ T helper (Th) differentiation upon pathogen encounters. Here the authors use fluorescently-labeled bacteria, helminth and fungi to track and describe the functions of IRF4+ migratory type 2 dendritic cells and monocytes in the specific induction of Th1, Th2 or Th17 responses following skin inoculation.
Antigen (Ag)-presenting cells (APC) instruct CD4+ helper T (Th) cell responses, but it is unclear whether different APC subsets contribute uniquely in determining Th differentiation in pathogen-specific settings. Here, we use skin-relevant, fluorescently-labeled bacterial, helminth or fungal pathogens to track and characterize the APC populations that drive Th responses in vivo. All pathogens are taken up by a population of IRF4+ dermal migratory dendritic cells (migDC2) that similarly upregulate surface co-stimulatory molecules but express pathogen-specific cytokine and chemokine transcripts. Depletion of migDC2 reduces the amount of Ag in lymph node and the development of IFNγ, IL-4 and IL-17A responses without gain of other cytokine responses. Ag+ monocytes are an essential source of IL-12 for both innate and adaptive IFNγ production, and inhibit follicular Th cell development. Our results thus suggest that Th cell differentiation does not require specialized APC subsets, but is driven by inducible and pathogen-specific transcriptional programs in Ag+ migDC2 and monocytes.Antigen presenting cells induce CD4+ T helper (Th) differentiation upon pathogen encounters. Here the authors use fluorescently-labeled bacteria, helminth and fungi to track and describe the functions of IRF4+ migratory type 2 dendritic cells and monocytes in the specific induction of Th1, Th2 or Th17 responses following skin inoculation.
ArticleNumber 5637
Author Hilligan, Kerry L.
Mayer, Johannes U.
Tang, Shiau-Choot
Connor, Lisa M.
Hyde, Evelyn J.
Ronchese, Franca
Yang, Jianping
Schmidt, Alfonso J.
Wakelin, Kirsty A.
MacDonald, Andrew S.
Roussel, Elsa
Sher, Alan
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/33159073$$D View this record in MEDLINE/PubMed
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SSID ssj0000391844
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Snippet Antigen (Ag)-presenting cells (APC) instruct CD4+ helper T (Th) cell responses, but it is unclear whether different APC subsets contribute uniquely in...
Antigen presenting cells induce CD4+ T helper (Th) differentiation upon pathogen encounters. Here the authors use fluorescently-labeled bacteria, helminth and...
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pubmedcentral
proquest
crossref
pubmed
springer
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Index Database
Publisher
StartPage 5637
SubjectTerms 13
13/21
13/31
631/250/1619/554/1898
631/250/21/1293
631/250/2499
631/250/2504/133
64/110
64/60
Animals
Antigen-presenting cells
Antigen-Presenting Cells - immunology
Antigens
CD4 antigen
Cell Differentiation
Cell migration
Chemokines
Cytokines
Dendritic cells
Dendritic Cells - immunology
Dendritic structure
Depletion
Differentiation (biology)
Female
Fungi
Helper cells
Humanities and Social Sciences
Inoculation
Interferon regulatory factor 4
Interferon Regulatory Factors - genetics
Interferon Regulatory Factors - immunology
Interferon-gamma - genetics
Interferon-gamma - immunology
Interleukin 12
Interleukin 4
Interleukin-17 - genetics
Interleukin-17 - immunology
Interleukin-4 - genetics
Interleukin-4 - immunology
Lymph nodes
Lymphocyte Activation
Lymphocytes T
Male
Mice
Mice, Inbred C57BL
Monocytes
Monocytes - cytology
Monocytes - immunology
multidisciplinary
Pathogens
Science
Science (multidisciplinary)
Skin
Skin - immunology
T-Lymphocytes, Helper-Inducer - cytology
T-Lymphocytes, Helper-Inducer - immunology
Transcription
γ-Interferon
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Title Dermal IRF4+ dendritic cells and monocytes license CD4+ T helper cells to distinct cytokine profiles
URI https://link.springer.com/article/10.1038/s41467-020-19463-9
https://www.ncbi.nlm.nih.gov/pubmed/33159073
https://www.proquest.com/docview/2471541064
https://search.proquest.com/docview/2458723546
https://pubmed.ncbi.nlm.nih.gov/PMC7647995
https://doaj.org/article/d65f3d80f398424cae180d6d1bb01a61
Volume 11
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