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T Cell Types and Functions

T Cell Types and Functions

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: Apr 28, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

IL-17 promotes murine lupus.

Gil Amarilyo¹, Elaine V Lourenço¹, Fu-Dong Shi²

¹Division of Rheumatology, Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90095; and.

Journal of Immunology (Baltimore, Md. : 1950)

|June 13, 2014

Summary

Interleukin-17 (IL-17) drives systemic lupus erythematosus (SLE) development in mice. Blocking IL-17 protected against lupus autoantibodies and kidney inflammation, suggesting IL-17 blockade as a potential SLE therapy.

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Last Updated: Apr 28, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

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Published on: September 26, 2013

Detection and Isolation of Viable Mouse IL-17-Secreting T Cells

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The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice

Published on: November 1, 2015

Area of Science:

Immunology
Autoimmune Diseases
Rheumatology

Background:

Th17 cells produce IL-17, a cytokine implicated in autoimmune disease pathogenesis.
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with complex mechanisms.

Purpose of the Study:

To investigate the direct role of IL-17 in the pathogenesis of SLE.
To evaluate the therapeutic potential of IL-17 blockade in SLE.

Main Methods:

Induction of SLE in IL-17-sufficient (wild-type) and IL-17-deficient mice using pristane.
Analysis of autoantibody production, glomerulonephritis, and T cell populations (including double-negative T cells and regulatory T cells).
Assessment of the role of Stat-1 signaling in SLE development.

Main Results:

IL-17-deficient mice were protected from pristane-induced SLE.
Protection was associated with reduced autoantibodies and glomerulonephritis.
IL-17 deficiency led to decreased double-negative T cells and increased regulatory T cells, independent of Stat-1 signaling.

Conclusions:

IL-17 plays a critical role in the pathogenesis of SLE.
These findings support IL-17 blockade as a promising therapeutic strategy for SLE.