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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...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
Antigen Processing Pathways01:31

Antigen Processing Pathways

MHC molecules are key players in the immune response, enabling T cells to recognize and respond to specific antigens. They are present on the surface of all nucleated cells in the body and are instrumental in presenting antigens to T cells and activating them. T cells recognize the MHC-antigen complex and initiate an immune response. MHC class I and MHC class II are two main types of MHC molecules, each associated with a distinct antigen processing pathway.
MHC Class I: Presenting Endogenous...
Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...

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Related Experiment Video

Updated: Jun 12, 2026

In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse
07:46

In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse

Published on: October 25, 2024

EAE mediated by a non-IFN-γ/non-IL-17 pathway.

Mark A Kroenke1, Stephen W Chensue, Benjamin M Segal

  • 1Holtom-Garrett Program in Neuroimmunology, Department of Neurology, University of Michigan, Ann Arbor, MI, USA.

European Journal of Immunology
|June 12, 2010
PubMed
Summary

Interferon-gamma (IFN-γ) and Interleukin-17 (IL-17) play distinct roles in experimental autoimmune encephalomyelitis (EAE). Their specific functions depend on the disease model and affected central nervous system regions.

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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

Related Experiment Videos

Last Updated: Jun 12, 2026

In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse
07:46

In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse

Published on: October 25, 2024

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

Area of Science:

  • Neuroimmunology
  • Autoimmune Diseases
  • T cell-mediated inflammation

Background:

  • Experimental autoimmune encephalomyelitis (EAE) is a T cell-mediated autoimmune disease model of multiple sclerosis.
  • Previous studies suggested redundancy between IFN-γ (Th1) and IL-17 (Th17) in EAE pathogenesis.
  • Mice lacking either IFN-γ or IL-17 are still susceptible to EAE, questioning their individual roles.

Purpose of the Study:

  • To investigate the distinct roles of IFN-γ and IL-17 in EAE pathogenesis.
  • To understand the cytokine requirements in different EAE models and CNS compartments.

Main Methods:

  • Adoptive transfer of IFN-γ-deficient effector T cells in C57BL/6 mice.
  • Induction of EAE using myelin antigens in Complete Freund's Adjuvant (CFA).
  • Analysis of central nervous system (CNS) inflammation and cytokine signaling pathways.

Main Results:

  • IFN-γ-deficient EAE required IL-17 signaling for brainstem inflammation.
  • Classical EAE (spinal cord inflammation) occurred without IFN-γ and IL-17 but depended on GM-CSF and CXCR2.
  • Cytokine importance varies across different CNS autoimmunity models.

Conclusions:

  • IFN-γ and IL-17 have non-redundant, context-dependent roles in EAE.
  • GM-CSF and CXCR2 are crucial for classical EAE in the absence of IFN-γ and IL-17.
  • Cytokine signaling pathways differentially regulate autoimmune inflammation in the CNS.