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Mesenchymal Stem Cells

Mesenchymal Stem Cells

Mesenchymal stem cells (MSCs) are adult stem cells that can differentiate into most connective tissue cell types, except for hematopoietic cells, depending upon the source of MSCs. For example, bone-marrow-derived MSCs (BM-MSCs) can differentiate into osteocytes, hepatocytes, and pancreatic and neuronal cells. MSCs can be isolated from various sources such as bone marrow, placenta, adipose tissue, teeth, and Wharton’s jelly, a gelatinous substance in the umbilical cord. The ease of their...

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Related Experiment Video

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Retroviral Overexpression of CXCR4 on Murine B-1a Cells and Adoptive Transfer for Targeted B-1a Cell Migration to the Bone Marrow and IgM Production

Retroviral Overexpression of CXCR4 on Murine B-1a Cells and Adoptive Transfer for Targeted B-1a Cell Migration to the Bone Marrow and IgM Production

Published on: May 31, 2020

CXCR5-Overexpressing Mesenchymal Stromal Cells Exhibit Enhanced Homing and Can Decrease Contact Hypersensitivity.

Xiaoran Zhang¹, Weijun Huang², Xiaoyong Chen¹

¹Biotherapy Center, Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510275, China; Center for Stem Cell Biology and Tissue Engineering, Key Laboratory for Stem Cells and Tissue Engineering, Ministry of Education, Sun Yat-Sen University, Guangzhou 510275, China.

Molecular Therapy : the Journal of the American Society of Gene Therapy

|April 30, 2017

Summary

Genetically engineered mesenchymal stromal cells (MSCs) overexpressing CXCR5 show enhanced migration to injured tissues. This improved homing significantly boosts their therapeutic efficacy in treating inflammatory conditions like contact hypersensitivity.

Keywords:

CXCR5 contact hypersensitivity homing immunomodulation mesenchymal stromal cells

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Published on: March 28, 2025

Area of Science:

Immunology
Regenerative Medicine
Cell Therapy

Background:

Mesenchymal stromal cells (MSCs) show therapeutic potential for tissue regeneration and immunomodulation.
Enhancing MSC migration to injured sites is crucial for improving cell-based therapy efficacy.
CXCL13 is significantly upregulated in injured tissues, but MSCs lack its receptor, CXCR5.

Purpose of the Study:

To engineer MSCs overexpressing CXCR5 (MSC^CXCR5) to enhance their migratory properties.
To evaluate the therapeutic efficacy of MSC^CXCR5 in a mouse model of contact hypersensitivity (CHS).

Main Methods:

Generated MSC^CXCR5, confirming retention of proliferation, differentiation, and immunomodulatory functions.
Assessed MSC^CXCR5 migration towards CXCL13 in vitro.
Utilized a mouse model of CHS to evaluate the in vivo therapeutic effects of MSC^CXCR5 infusion.

Main Results:

MSC^CXCR5 exhibited significantly increased migration towards CXCL13.
Systemic infusion of MSC^CXCR5 dramatically suppressed CHS, reducing inflammatory cell infiltration and pro-inflammatory cytokine production.
Administered MSC^CXCR5 localized to inflamed tissues, inhibited T cell proliferation, promoted T cell apoptosis, and suppressed T cell-derived inflammatory factors.

Conclusions:

CXCR5 overexpression enhances MSCs' response to migratory cues, improving their homing to inflamed tissues.
Engineered MSC^CXCR5 demonstrate intensified immunomodulatory effects in vivo.
Targeted enhancement of stem/progenitor cell homing via CXCR5 overexpression offers a promising strategy to improve MSC-based therapies.