Th17 Signaling
Th17 Signaling - Related Videos
01:56
Inducing Paralysis in a Mouse Model via Transfer of Aquaporin-4-Specific Th17 Cells
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2025
This video demonstrates the procedure of inducing paralysis by transferring activated Th17 cells targeting aquaporin-4 into a mouse model. In the central nervous system, the activated Th17 cells interact with aquaporin-4-expressing astrocytes, triggering an immune response that leads to tail and limb paralysis in the mouse.
10:15
Small RNA Transfection in Primary Human Th17 Cells by Next Generation Electroporation
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Cited by 5 •
2017
Next generation electroporation is an efficient method for transfecting human Th17 cells with small RNAs to alter gene expression and cell behavior.
12:59
Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
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Cited by 33 •
2013
With effector functions distinct from other T cell subsets, Th17 cells have been centrally implicated in inflammatory autoimmunity. This in vitro Th17 differentiation protocol provides a means to determine whether naïve CD4+ T lymphocytes can differentiate into Th17 cells, and to further examine their role in autoimmunity and host response.
08:02
Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice
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Cited by 11 •
2015
Although Candida infection models are available to study host immune resistance, a model to study T cell mediated immunopathology in the context of Candida infection is absent. Here we describe a method to establish Th17 immunopathology associated with oral Candida infection in immunodeficient mice.
07:46
In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse
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Cited by 1 •
2024
This protocol describes the differentiation of naïve CD4+ T cells into pathogenic Th17 cells in vitro. Specifically, when combined with a multi-parameter flow cytometry-based approach, 90% purity of pathogenic Th17 cells can be obtained from naïve CD4+ T cells using this differentiation method.
FAQs
Transforming growth factor-β and interleukin-6 act during naïve CD4+ T-cell differentiation to promote the transcription factor RORγt through STAT3. This molecular sequence helps establish the Th17-cell program rather than merely activating already differentiated cells. Studying these signals clarifies how cytokine environments influence immune-cell development at barrier tissues.
Interleukin-23 supports Th17-cell maintenance and expansion after the differentiation process has been initiated. This gives the pathway a continuing regulatory phase, in addition to its early developmental signals from transforming growth factor-β and interleukin-6. The distinction helps researchers examine whether a response reflects Th17-cell formation, persistence, or increased abundance.
Th17 cells produce IL-17A, IL-17F, and IL-22, which connect their differentiation state to defense at barrier tissues. These cytokines help coordinate neutrophil recruitment and strengthen epithelial defenses against extracellular microbes. Measuring their production therefore provides information about the functional output of Th17 signaling, rather than only its upstream transcriptional regulation.
In infection research, the pathway is examined because Th17-cell activity links cytokine regulation with two protective outcomes: recruiting neutrophils and reinforcing epithelial defenses. These effects are especially relevant at barrier tissues exposed to extracellular microbes. Investigators can therefore use Th17 signaling as a framework for relating immune-cell behavior to host defense mechanisms.
Studies can examine several connected outcomes, including the development of Th17 cells from naïve CD4+ T cells, their maintenance and expansion, production of IL-17A, IL-17F, and IL-22, neutrophil recruitment, and epithelial defense. Considering these stages together helps distinguish altered differentiation from changes in persistence or downstream immune activity.
Th17 signaling supports protection against extracellular microbes, but dysregulated activity can also contribute to inflammatory and autoimmune disease. This opposing relationship makes the pathway a therapeutic investigation target: researchers seek to understand how its protective functions relate to harmful inflammation. The scientific challenge is to interpret pathway activity in the context of both host defense and disease.