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Related Experiment Video

Updated: Jun 26, 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

CXCL10 and autoimmune diseases.

Eun Young Lee¹, Zang-Hee Lee, Yeong Wook Song

¹Division of Rheumatology, Department of Internal Medicine, Seoul National University College of Medicine, Republic of Korea.

Autoimmunity Reviews

|December 25, 2008

Summary

Chemokine CXCL10 (C-X-C motif chemokine ligand 10) and its receptor CXCR3 are implicated in autoimmune diseases. Our study reveals CXCL10

Area of Science:

Immunology
Rheumatology
Molecular Biology

Background:

Chemokine (C-X-C motif) ligand 10 (CXCL10) is a Th1-chemokine that binds to receptor CXCR3.
CXCL10 regulates immune responses by activating and recruiting leukocytes like T cells, eosinophils, and monocytes.
Elevated CXCL10 and CXCR3 expression is observed in various autoimmune diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), Sjogren syndrome (SS), systemic sclerosis (SSc), and idiopathic inflammatory myopathy (IIM).

Purpose of the Study:

To investigate the role of CXCL10 in autoimmune diseases.
To explore the pathogenic mechanisms of CXCL10 in bone destruction in RA.
To identify potential therapeutic targets within the CXCL10/CXCR3 pathway.

Main Methods:

Analysis of serum and tissue expression of CXCL10.

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

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Published on: May 8, 2016

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

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Investigation of CXCL10's role in leukocyte recruitment and homing.

Assessment of CXCL10-induced receptor activator of NF-kappaB ligand (RANKL) in RA synovial tissue.

Main Results:

CXCL10 expression is increased in multiple autoimmune diseases.
CXCL10 and CXCR3 contribute to leukocyte homing and inflammation perpetuation.
CXCL10 induces RANKL in RA synovial tissue, suggesting a role in bone destruction.

Conclusions:

CXCL10 plays a significant pathogenic role in autoimmune diseases, including bone destruction in RA.
CXCL10 exhibits pleiotropic functions beyond its chemotactic effects.
Targeting the CXCL10/CXCR3 axis and its interactions may offer therapeutic strategies for autoimmune conditions.