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Updated: Jun 15, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 26, 2013

Th17 cells in autoimmune demyelinating disease.

Benjamin Matthew Segal¹

¹Multiple Sclerosis Center, University of Michigan, Ann Arbor, 48109-2200, USA. bmsegal@unich.edu

Seminars in Immunopathology

|March 3, 2010

Summary

Studies link T helper 17 (Th17) cells to demyelinating plaques in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). Interleukin-17A (IL-17A) deficiency partially reduces EAE, suggesting complex roles in autoimmune demyelination.

Area of Science:

Neuroimmunology
Autoimmune Diseases
Cellular Immunology

Background:

Published studies indicate a correlation between Th17 cell accumulation and demyelinating plaque development in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE).
Establishing a direct causal link between Th17 cells and disease pathogenesis has been challenging.
Previous research shows that Interleukin-17A (IL-17A) deficiency or neutralization only attenuates, not eliminates, EAE, hinting at alternative pathogenic mechanisms.

Purpose of the Study:

To investigate the role of Th17 cells and IL-17A in autoimmune demyelination.
To explore the potential of IL-17A as a biomarker for neuroinflammation and plaque formation in MS.

Main Methods:

Review of recent studies on multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE).

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Analysis of data concerning Th17 cell infiltration and IL-17A levels in the central nervous system and periphery.

Evaluation of the impact of IL-17A deficiency or neutralization on EAE severity.

Main Results:

Th17 cells are associated with demyelinating plaque formation in MS and EAE models.
IL-17A plays a role in EAE, but its absence does not completely halt the disease.
Evidence suggests distinct T cell lineages can drive similar autoimmune demyelinating diseases with varying IL-17A dependence.

Conclusions:

The complex role of IL-17A in autoimmune demyelination raises questions about the efficacy of IL-17A targeted therapies for MS.
IL-17A expression in peripheral blood mononuclear cells may serve as a valuable surrogate biomarker for neuroinflammation and plaque formation.
IL-17A could be a useful outcome measure in future clinical trials for MS and related conditions.