Th17 Cells
Th17 Cells - Related Videos
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.
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.
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.
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.
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.
FAQs
Th17-cell differentiation depends on the cytokine environment surrounding a naïve CD4+ T cell. Transforming growth factor beta and interleukin-6 provide signals that drive the cell toward the Th17 pathway. This signaling context helps explain how precursor T cells acquire Th17-associated functions and gives immunology researchers a basis for examining the conditions that promote this lineage.
RORγt acts as a transcription factor that promotes the Th17 gene program. By supporting expression of genes associated with this lineage, it helps establish the cellular program connected to interleukin-17 secretion. Its role links differentiation signals to the functional output of Th17 cells, making RORγt an important molecular feature when researchers analyze how these cells develop.
Interleukin-17 acts on epithelial and stromal cells at barrier tissues. These target cells respond by recruiting neutrophils and strengthening antimicrobial responses, connecting T-cell activity with local innate defense. This pathway is especially relevant at mucosal surfaces, where coordinated epithelial, stromal, and immune responses help protect against extracellular pathogens.
Their importance comes from the downstream effects of interleukin-17 rather than from cytokine production alone. By stimulating epithelial and stromal cells to recruit neutrophils and enhance antimicrobial responses, Th17-associated activity helps organize defense against pathogens located outside host cells. This relationship makes the cells a useful focus for studying protective immunity at mucosal barriers.
Th17 cells are relevant because the same immune pathways associated with host defense can also be examined in the context of inflammatory and autoimmune disease. Their differentiation program, RORγt activity, and interleukin-17 secretion provide connected features for investigating immune regulation. This research can clarify disease mechanisms and support development of therapeutic strategies directed at these pathways.
Therapeutic interest follows from the defined connection between Th17-cell biology and immune outcomes. Researchers can consider the differentiation signals, RORγt-driven gene program, or interleukin-17-related effects when exploring ways to influence immune responses. Such work may aim to preserve protective defense against extracellular pathogens while addressing inflammatory or autoimmune processes associated with Th17 activity.