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Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
Published on: September 26, 2013
Mechanisms controlling Th17 cytokine expression and host defense
Jeremy P McAleer1, Jay K Kolls
1Department of Genetics, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
Journal of Leukocyte Biology
|April 14, 2011
Summary
T helper 17 (Th17) cells are crucial for mucosal immunity and tissue repair, responding to microbiota and environmental cues. These adaptable CD4 T cells, along with innate cells, produce IL-17 and IL-22 to combat pathogens.
Area of Science:
- Immunology
- Microbiology
- Cellular Biology
Background:
- T helper 17 (Th17) cells are vital for mucosal immunity, orchestrating responses like antimicrobial peptide production and tissue repair.
- Commensal microbiota and aryl hydrocarbon receptor (Ahr) ligands influence Th17 cell differentiation and gene expression.
- Epigenetic modifications and transcription factor plasticity allow Th17 cells to adapt to diverse microenvironments.
Purpose of the Study:
- To elucidate the multifaceted roles of Th17 cells in mucosal immunity.
- To explore the regulatory mechanisms governing Th17 cell polarization and function.
- To understand the interactions between Th17 cells and other immune and non-immune cells.
Main Methods:
- Analysis of gene expression and epigenetic changes during Th17 cell differentiation.
- Investigation of the impact of microbiota and Ahr ligands on Th17 cells.
- Characterization of cytokine production by both CD4+ T cells and innate immune cells.
- Identification of cellular targets of IL-17 and IL-22.
Main Results:
- Th17 cells stimulate epithelial cells to produce antimicrobial peptides and promote neutrophil recruitment.
- Environmental factors like microbiota and Ahr ligands stabilize Th17 cell gene expression.
- Epigenetic changes enhance the accessibility of key cytokine gene loci (il17a, il17f, il22).
- Th17 cells exhibit plasticity, retaining potential to express T-bet, Foxp3, or GATA-3.
- Innate cells (γδ T cells, NK cells, LTi cells) are early sources of IL-17 and IL-22 in IL-23-driven responses.
- IL-17 targets epithelial cells, fibroblasts, macrophages, and B cells, contributing to pathogen defense.
Conclusions:
- Th17 cells are central players in mucosal immunity, integrating environmental signals for effective host defense.
- The plasticity and diverse cellular interactions of Th17 cells highlight their adaptability in combating various pathogens.
- Understanding Th17 cell biology is crucial for developing strategies against infectious and inflammatory diseases.
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