hUCB-MSCs in Disease Models - WHOLE BODY STEM CELL™

hUCB-MSCs: A Versatile Therapeutic

Human Umbilical Cord Blood-Derived Mesenchymal Stem Cells (hUCB-MSCs) offer a fascinating source for cell therapy with unique capabilities for regeneration, immune modulation, and targeted delivery.

Why hUCB-MSCs?

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Hypo-Immunogenic

hUCB-MSCs possess a primitive character that results in lower immunogenicity compared to bone marrow MSCs.

Low Expression: Lack MHC-II and co-stimulatory molecules (CD40, CD80, CD86).
HLA Mismatch Tolerance: Allows for greater HLA mismatch without inducing Graft vs. Host Disease (GVHD).
Safe Transplantation: Can be successfully transplanted as allogeneic ("off-the-shelf") products.

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Immune Regulation

They actively suppress immune responses through cell-to-cell contact and soluble factors.

Suppression: Inhibits lymphocyte proliferation and mature dendritic cell function.
Induction: Increases the portion of Regulatory T cells (Tregs).
Factors: Involves IDO (Indoleamine 2,3-dioxygenase), PGE2, and HLA-G.

Therapeutic Potential in Disease Models

Cartilage Regeneration

Target: Osteoarthritis (OA) & Rheumatoid Arthritis (RA)

hUCB-MSCs have superior chondrogenic differentiation potential.

Mechanism: Differentiation into cartilage tissue + Paracrine anti-inflammatory effects (e.g., Thrombospondin-1/2 suppressing IFN-γ/TNF-α).

Glioma Therapy

Target: Brain Tumors

MSCs exhibit "tumor tropism," migrating specifically toward glioma cells.

Mechanism: Attracted by IL-8 secreted by tumors. Can deliver therapeutic agents like TRAIL (Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand) to kill cancer cells.

Ischemic Brain Damage

Target: Stroke

Promotes behavioral recovery and reduces infarct volume.

Mechanism: Differentiation into neurons/astrocytes + "Nursing Effect" via secretion of BDNF (Brain-Derived Neurotrophic Factor) and VEGF (Vascular Endothelial Growth Factor).

Lung Diseases

Target: Acute Lung Injury & Fibrosis

Reduces inflammation, fibrosis, and collagen deposition.

Mechanism: Decreases inflammatory cytokines (TNF-α, IL-6) and fibrotic markers (TGF-β, collagen). Differentiates into lung epithelial cells.

Liver Diseases

Target: Cirrhosis

Prevents hepatocyte cell death and stimulates proliferation.

Mechanism: Expresses hepatocyte markers (human albumin, α-fetoprotein). Inhibits TGF-β1 and collagen type I expression to reduce scarring.

Core Mechanisms of Action

Beyond Regeneration

While early research focused on direct tissue regeneration, recent evidence highlights the "Paracrine" or "Nursing Effect" as a primary driver of therapeutic efficacy.

Differentiation: Replacing damaged cells (chondrocytes, neurons, hepatocytes).
Immune Modulation: Suppressing inflammation and rejection.
Nursing Effect: Secreting growth factors (BDNF, VEGF) to support host tissue.
Tropism: Migrating specifically to sites of injury or tumors.

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