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Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

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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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Related Experiment Video

Updated: Nov 17, 2025

Study of Dendritic Cell Development by Short Hairpin RNA-Mediated Gene Knockdown in a Hematopoietic Stem and Progenitor Cell Line In vitro
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IL-27 Negatively Regulates Tip-DC Development during Infection.

Gongguan Liu1,2, Osama Abas1,2, Yong Fu1,2

  • 1Division of Immunology, Virginia-Maryland College of Veterinary Medicine, University of Maryland, College Park, Maryland, USA.

Mbio
|February 17, 2021
PubMed
Summary
This summary is machine-generated.

Interleukin-27 receptor (IL-27R) signaling normally prevents excessive tumor necrosis factor/inducible nitric oxide synthase-producing dendritic cell (Tip-DC) development. Blocking IL-27R exacerbates Tip-DC formation, leading to liver injury and increased mortality during African trypanosome infections.

Keywords:
African trypanosomesIFN-γIL-27Ly6C+ monocytesLy6C− monocytesTip-DCshost-pathogen interactionsintravital imagingliver immunitymurine model of African trypanosomiasisparasites

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Area of Science:

  • Immunology
  • Cell Biology
  • Parasitology

Background:

  • Tumor necrosis factor/inducible nitric oxide synthase-producing dendritic cells (Tip-DCs) are crucial immune effectors during infections but can cause tissue damage when overproduced.
  • The regulatory mechanisms governing Tip-DC development are not fully understood, hindering the development of targeted therapies.
  • Interleukin-27 receptor (IL-27R) signaling plays a role in modulating immune responses, but its specific impact on Tip-DC differentiation requires elucidation.

Purpose of the Study:

  • To investigate the role of IL-27R signaling in regulating Tip-DC development during African trypanosome infection.
  • To elucidate the cellular and molecular mechanisms underlying Tip-DC differentiation in the absence of IL-27R signaling.
  • To determine the therapeutic potential of targeting IL-27 signaling for controlling Tip-DC-mediated pathology.

Main Methods:

  • Utilized a mouse model infected with African trypanosomes.
  • Analyzed the impact of IL-27R deficiency on monocyte populations (Ly6C+ and Ly6C-) and Tip-DC differentiation.
  • Investigated the involvement of CD4+ T cells, interferon-gamma (IFN-γ) signaling, and monocyte-intrinsic pathways in Tip-DC development.

Main Results:

  • IL-27R deficiency led to increased intrahepatic accumulation of Ly6C+ monocytes and their differentiation into pathogenic Tip-DCs.
  • A CD4+ T cell-IFN-γ axis, acting via cell-intrinsic IFN-γ signaling, drove Ly6C+ monocyte differentiation into Tip-DCs.
  • Hyperactive IFN-γ signaling also caused Ly6C- monocyte death, removing their negative regulatory effect on Tip-DC development.

Conclusions:

  • IL-27 negatively regulates Tip-DC development through a dual-track mechanism involving CD4+ T cells and monocytes, preventing excessive Tip-DC-mediated pathology.
  • IL-27 signaling inhibits Tip-DC expansion by counteracting the cell-intrinsic effects of IFN-γ on both Ly6C+ and Ly6C- monocytes.
  • Targeting IL-27 signaling represents a potential therapeutic strategy to modulate Tip-DC development and mitigate tissue damage in parasitic infections.