Antigen presentation by dendritic cells and their instruction of CD4+ T helper cell responses

Dendritic cells are powerful antigen-presenting cells that are essential for the priming of T cell responses. In addition to providing T-cell-receptor ligands and co-stimulatory molecules for naive T cell activation and expansion, dendritic cells are thought to also provide signals for the different...

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Bibliographic Details
Published inCellular & molecular immunology Vol. 17; no. 6; pp. 587 - 599
Main Authors Hilligan, Kerry L., Ronchese, Franca
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 01.06.2020
Nature Publishing Group
Subjects
631/250/1619/554/1898
631/250/21/1566
631/250/2152/1566/2493
631/250/2504/133/2505
Antibodies
Antigen presentation
Antigen-presenting cells
Antigens
Biomedical and Life Sciences
Biomedicine
CD4 antigen
Cell activation
Cell differentiation
Chemokines
Cytokines
Dendritic cells
Effector cells
Helper cells
Immunology
Interfaces
Ligands
Lymphocytes
Lymphocytes T
Medical Microbiology
Microbiology
Phenotypes
Review
Review Article
Toll-like receptors
Transcription
Vaccine
Th effector responses
dendritic cells
CD4+ T cells
Online AccessGet full text

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Abstract Dendritic cells are powerful antigen-presenting cells that are essential for the priming of T cell responses. In addition to providing T-cell-receptor ligands and co-stimulatory molecules for naive T cell activation and expansion, dendritic cells are thought to also provide signals for the differentiation of CD4+ T cells into effector T cell populations. The mechanisms by which dendritic cells are able to adapt and respond to the great variety of infectious stimuli they are confronted with, and prime an appropriate CD4+ T cell response, are only partly understood. It is known that in the steady-state dendritic cells are highly heterogenous both in phenotype and transcriptional profile, and that this variability is dependent on developmental lineage, maturation stage, and the tissue environment in which dendritic cells are located. Exposure to infectious agents interfaces with this pre-existing heterogeneity by providing ligands for pattern-recognition and toll-like receptors that are variably expressed on different dendritic cell subsets, and elicit production of cytokines and chemokines to support innate cell activation and drive T cell differentiation. Here we review current information on dendritic cell biology, their heterogeneity, and the properties of different dendritic cell subsets. We then consider the signals required for the development of different types of Th immune responses, and the cellular and molecular evidence implicating different subsets of dendritic cells in providing such signals. We outline how dendritic cell subsets tailor their response according to the infectious agent, and how such transcriptional plasticity enables them to drive different types of immune responses.
AbstractList Dendritic cells are powerful antigen-presenting cells that are essential for the priming of T cell responses. In addition to providing T-cell-receptor ligands and co-stimulatory molecules for naive T cell activation and expansion, dendritic cells are thought to also provide signals for the differentiation of CD4+ T cells into effector T cell populations. The mechanisms by which dendritic cells are able to adapt and respond to the great variety of infectious stimuli they are confronted with, and prime an appropriate CD4+ T cell response, are only partly understood. It is known that in the steady-state dendritic cells are highly heterogenous both in phenotype and transcriptional profile, and that this variability is dependent on developmental lineage, maturation stage, and the tissue environment in which dendritic cells are located. Exposure to infectious agents interfaces with this pre-existing heterogeneity by providing ligands for pattern-recognition and toll-like receptors that are variably expressed on different dendritic cell subsets, and elicit production of cytokines and chemokines to support innate cell activation and drive T cell differentiation. Here we review current information on dendritic cell biology, their heterogeneity, and the properties of different dendritic cell subsets. We then consider the signals required for the development of different types of Th immune responses, and the cellular and molecular evidence implicating different subsets of dendritic cells in providing such signals. We outline how dendritic cell subsets tailor their response according to the infectious agent, and how such transcriptional plasticity enables them to drive different types of immune responses.
Dendritic cells are powerful antigen-presenting cells that are essential for the priming of T cell responses. In addition to providing T-cell-receptor ligands and co-stimulatory molecules for naive T cell activation and expansion, dendritic cells are thought to also provide signals for the differentiation of CD4+ T cells into effector T cell populations. The mechanisms by which dendritic cells are able to adapt and respond to the great variety of infectious stimuli they are confronted with, and prime an appropriate CD4+ T cell response, are only partly understood. It is known that in the steady-state dendritic cells are highly heterogenous both in phenotype and transcriptional profile, and that this variability is dependent on developmental lineage, maturation stage, and the tissue environment in which dendritic cells are located. Exposure to infectious agents interfaces with this pre-existing heterogeneity by providing ligands for pattern-recognition and toll-like receptors that are variably expressed on different dendritic cell subsets, and elicit production of cytokines and chemokines to support innate cell activation and drive T cell differentiation. Here we review current information on dendritic cell biology, their heterogeneity, and the properties of different dendritic cell subsets. We then consider the signals required for the development of different types of Th immune responses, and the cellular and molecular evidence implicating different subsets of dendritic cells in providing such signals. We outline how dendritic cell subsets tailor their response according to the infectious agent, and how such transcriptional plasticity enables them to drive different types of immune responses.
Author Hilligan, Kerry L.
Ronchese, Franca
Author_xml – sequence: 1
  givenname: Kerry L.
  orcidid: 0000-0003-1238-1552
  surname: Hilligan
  fullname: Hilligan, Kerry L.
  organization: Malaghan Institute of Medical Research, Immunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health
– sequence: 2
  givenname: Franca
  orcidid: 0000-0001-5835-8230
  surname: Ronchese
  fullname: Ronchese, Franca
  email: fronchese@malaghan.org.nz
  organization: Malaghan Institute of Medical Research
BackLink https://www.ncbi.nlm.nih.gov/pubmed/32433540$$D View this record in MEDLINE/PubMed
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Snippet Dendritic cells are powerful antigen-presenting cells that are essential for the priming of T cell responses. In addition to providing T-cell-receptor ligands...
Dendritic cells are powerful antigen-presenting cells that are essential for the priming of T cell responses. In addition to providing T-cell-receptor ligands...
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SubjectTerms 631/250/1619/554/1898
631/250/21/1566
631/250/2152/1566/2493
631/250/2504/133/2505
Antibodies
Antigen presentation
Antigen-presenting cells
Antigens
Biomedical and Life Sciences
Biomedicine
CD4 antigen
Cell activation
Cell differentiation
Chemokines
Cytokines
Dendritic cells
Effector cells
Helper cells
Immunology
Interfaces
Ligands
Lymphocytes
Lymphocytes T
Medical Microbiology
Microbiology
Phenotypes
Review
Review Article
Toll-like receptors
Transcription
Vaccine
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Title Antigen presentation by dendritic cells and their instruction of CD4+ T helper cell responses
URI https://link.springer.com/article/10.1038/s41423-020-0465-0
https://www.ncbi.nlm.nih.gov/pubmed/32433540
https://www.proquest.com/docview/2408526612
https://search.proquest.com/docview/2405324517
https://pubmed.ncbi.nlm.nih.gov/PMC7264306
Volume 17
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