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Related Concept Videos

T Cell Types and Functions01:24

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...
Lymphoid Cells and Tissues01:18

Lymphoid Cells and Tissues

Lymphoid cells and tissues are integral to the immune system, which is crucial in maintaining our body's defense against harmful pathogens. They form the building blocks of lymphoid organs, which include the spleen, thymus, and lymph nodes.
Lymphoid cells consist of various types of immune system cells. These include B and T lymphocytes, which are responsible for producing antibodies and killing infected cells, respectively. Dendritic cells act as messengers between the innate and adaptive...
B Cell Activation and Differentiation01:24

B Cell Activation and Differentiation

The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...

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Related Experiment Video

Updated: May 29, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
12:59

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

A novel pro-lymphangiogenic function for Th17/IL-17.

Sunil K Chauhan1, Yiping Jin, Sunali Goyal

  • 1Department of Ophthalmology, Harvard Medical School, Boston, MA, USA. sunil.chauhan@schepens.harvard.edu

Blood
|September 13, 2011
PubMed
Summary

T helper 17 (Th17) cells and their cytokine, IL-17, directly promote lymphatic vessel growth (lymphangiogenesis) by increasing VEGF-D expression. Blocking IL-17 reduces lymphangiogenesis in autoimmune eye disease.

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Last Updated: May 29, 2026

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Published on: April 16, 2015

Area of Science:

  • Immunology
  • Vascular Biology

Background:

  • T helper 17 (Th17) cells and their cytokine, interleukin-17 (IL-17), are known for pro-inflammatory roles and inducing blood vessel growth (angiogenesis).
  • Their role in lymphatic vessel formation (lymphangiogenesis) remains less understood, particularly in the context of autoimmune diseases.

Purpose of the Study:

  • To elucidate the mechanisms by which IL-17 influences lymphangiogenesis.
  • To investigate the therapeutic potential of targeting IL-17 in autoimmune conditions characterized by Th17 cell activity.

Main Methods:

  • Utilized mouse cornea micropocket and cell culture assays to study IL-17's direct effects on lymphatic endothelial cells.
  • Analyzed the expression of prolymphangiogenic factors like VEGF-D.
  • Employed a preclinical mouse model of Th17-dominant autoimmune ocular disease to assess the in vivo impact of IL-17 blockade.

Main Results:

  • IL-17 directly stimulates lymphatic endothelial cell proliferation and upregulates VEGF-D expression, promoting lymphangiogenesis.
  • IL-17-induced blood vessel growth is primarily mediated by IL-1β secretion from responsive cells.
  • In vivo blockade of IL-17 significantly reduced corneal lymphangiogenesis and disease progression in the autoimmune model.

Conclusions:

  • IL-17 possesses a novel prolymphangiogenic function, distinct from its role in angiogenesis.
  • IL-17 contributes to the amplification of immune responses partly through the induction of lymphangiogenesis.
  • Targeting IL-17 may offer a therapeutic strategy for autoimmune diseases involving excessive lymphangiogenesis.