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Related Experiment Video

Updated: May 8, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues

Published on: May 8, 2016

Interferon Lambda Signaling Restrains Experimental Autoimmune Encephalomyelitis.

Mohammad Asif Sherwani¹, Samuel J Duesman¹, Zdenek Hel²

¹Department of Dermatology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.

|March 28, 2024

Summary

This summary is machine-generated.

Interferon-lambda (IFN-λ) signaling restrains autoimmune neuroinflammation by limiting neutrophil activation and central nervous system infiltration. This suggests IFN-λ as a potential therapeutic for multiple sclerosis.

Keywords:

interferon lambda multiple sclerosis neutrophils

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Last Updated: May 8, 2026

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Published on: March 26, 2019

Area of Science:

Immunology
Neuroscience
Autoimmunity

Background:

Type III interferons (IFN-λ) modulate immune responses.
Autoimmune neuroinflammation, such as experimental autoimmune encephalitis (EAE), involves complex immune cell interactions.
The role of IFN-λ in EAE pathogenesis remains incompletely understood.

Purpose of the Study:

To investigate the role of IFN-λ signaling in EAE development and progression.
To determine how IFN-λ influences T helper 1 (Th1) and T helper 17 (Th17) cell-mediated neuroinflammation.
To elucidate the impact of IFN-λ on neutrophil activation and central nervous system (CNS) infiltration in autoimmune conditions.

Main Methods:

Experimental autoimmune encephalitis (EAE) was induced in wild-type (WT) and IFNLR1 knockout (IFNLR1KO) mice.
Encephalitogenic Th1 and Th17 cells were generated and transferred into recipient mice.
In vitro assays assessed macrophage-mediated T cell expansion.
Flow cytometry analyzed immune cell populations in the spinal cord.

Main Results:

IFNLR1KO mice exhibited significantly more severe EAE than WT mice.
Encephalitogenic Th1 cells induced more severe EAE in IFNLR1KO recipients compared to WT.
IFNLR1KO macrophages promoted expansion of Th17 cells but not Th1 cells.
Activated neutrophils were increased in the spinal cords of EAE mice.

Conclusions:

IFN-λ signaling plays a protective role in autoimmune neuroinflammation.
IFN-λ restrains neutrophil activation and CNS migration, mitigating disease severity.
Targeting IFN-λ may offer a therapeutic strategy for multiple sclerosis with potentially fewer side effects.