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Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

3.3K
When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
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Isolation of Mouse Lung Dendritic Cells
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CD103(+) Dendritic Cells Control Th17 Cell Function in the Lung.

Teresa Zelante1, Alicia Yoke Wei Wong2, Tang Jing Ping3

  • 1Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A(∗)STAR), Singapore 138648, Singapore; Department of Experimental Medicine, University of Perugia, 06132 Perugia, Italy.

Cell Reports
|September 15, 2015
PubMed
Summary
This summary is machine-generated.

Lung dendritic cells (DCs) control T helper 17 (Th17) cell responses. Balancing IL-2 and IL-23 production by DCs is crucial for preventing hyperinflammation during pulmonary aspergillosis.

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Isolation and Characterization of Dendritic Cells and Macrophages from the Mouse Intestine
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Area of Science:

  • Immunology
  • Cellular Biology
  • Infectious Diseases

Background:

  • T helper 17 (Th17) cells play a critical role in host defense against pathogens and in autoimmune diseases.
  • The plasticity and regulation of Th17 cell functional programs, including their stem-cell-like properties, are not fully understood.
  • Signaling pathways governing Th17 cell plasticity remain largely undefined, particularly in the context of infection.

Purpose of the Study:

  • To investigate the role of dendritic cells (DCs) in regulating Th17 cell responses during invasive pulmonary aspergillosis.
  • To identify the specific signaling pathways and cytokines involved in controlling Th17 cell plasticity and inflammatory responses in the lungs.
  • To elucidate the balance between IL-2 and IL-23 production by lung DCs and its impact on infection outcomes.

Main Methods:

  • Utilized a mouse model of invasive pulmonary aspergillosis to study host-pathogen interactions.
  • Investigated the function of lung CD103(+) dendritic cells (DCs) and their cytokine production.
  • Analyzed the role of Nuclear Factor of Activated T-cells (NFAT) signaling in DC-mediated IL-2 production.
  • Assessed the impact of IL-2 deficiency in DCs on Th17 cell polarization, IL-23 production, and overall inflammatory response.

Main Results:

  • Lung CD103(+) dendritic cells (DCs) produce IL-2, dependent on NFAT signaling, which is essential for an optimal protective Th17 response.
  • Absence of IL-2 production by DCs leads to unrestrained IL-23 production and fatal hyperinflammation.
  • This hyperinflammation is characterized by strong Th17 polarization and the development of a Th17 stem-cell-like population.
  • The balance between IL-2 and IL-23 production by lung DCs is identified as a key regulator of the local inflammatory response to infection.

Conclusions:

  • The study identifies a critical role for IL-2 produced by lung dendritic cells in regulating Th17 cell responses during pulmonary aspergillosis.
  • The balance between IL-2 and IL-23 production by DCs is a key determinant of inflammatory severity and protective immunity.
  • These findings highlight a novel mechanism for controlling Th17 cell plasticity and offer potential therapeutic targets for inflammatory diseases.