Psoriasis is a chronic autoimmune disease in which the immune system mistakenly attacks the body’s own skin cells, causing inflammation, accelerated cell division, and the formation of characteristic plaques.
How Stem Cells Work in Psoriasis:
1. Immunomodulation
Mesenchymal stem cells (MSCs), typically derived from bone marrow, adipose tissue, umbilical cord blood, embryonic, or fetal material, have the ability to suppress overactive immune responses. They:
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Suppress the activity of T cells and dendritic cells — the main participants in the autoimmune attack;
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Promote the production of anti-inflammatory cytokines (e.g., IL-10);
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Reduce levels of pro-inflammatory factors such as TNF-α and IL-17, which play key roles in the pathogenesis of psoriasis.
2. Tissue Regeneration
MSCs can promote the healing of damaged skin by stimulating repair and remodeling processes.
3. Reduced Frequency of Relapses
Studies show that after MSC therapy, some patients experience long-term remission — a more stable condition without flare-ups.
What Are MUSE Cells and Why Are They Considered for Psoriasis Treatment
MUSE (Multilineage Differentiating Stress Enduring) cells are a special type of mesenchymal stem cell known for their stress resistance and ability to differentiate into various tissue types. They possess two key properties:
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Immunomodulation — able to induce anti-inflammatory responses and maintain immune balance.
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Tissue Regeneration — can transform into skin cells and repair damaged areas.
Organelles and Extracellular Vesicles (Exosomes, Micro- and Nanovesicles)
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Exosomes (tiny vesicles, ~30–150 nm) — a key mechanism of stem cell action: they carry proteins, microRNAs, and lipids that regulate inflammation, inhibit T cell activation, and accelerate skin regeneration.
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Vesicles derived from MSCs have been well studied in skin disease models (including psoriasis-like conditions), demonstrating reduced inflammation, normalized cytokine levels, and improved epidermal structure.
How Stem Cells Suppress T Cells: Mechanism of Action
Mesenchymal stem cells (MSCs) not only differentiate into various tissue types but also actively modulate the immune response, including suppression of T lymphocyte activity. This effect is especially important in the treatment of autoimmune diseases such as psoriasis.
🔹 Stages and Mechanisms of T Cell Suppression:
1. Secretion of Immunomodulatory Factors
MSCs secrete a range of substances that inhibit T cell proliferation and activation:
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TGF-β (Transforming Growth Factor-β) — inhibits Th1/Th17 activation, enhances regulatory T cells (Tregs);
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IL-10 (Interleukin 10) — anti-inflammatory cytokine, reduces IL-2 and IFN-γ production;
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IDO (Indoleamine 2,3-dioxygenase) — depletes tryptophan necessary for T cell growth;
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PGE2 (Prostaglandin E2) — suppresses Th1/Th17, activates Tregs;
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HLA-G — immunoregulatory molecule, inhibits cytotoxic T cells.
2. Contact-Dependent Suppression
MSCs also directly interact with T cells through surface molecules:
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PD-L1 (Programmed Death Ligand 1) on MSCs binds to PD-1 on T cells → induces apoptosis or anergy (inactivation) of T cells;
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Galectin-1 — binds to glycoproteins on T cells and induces their death.
3. Activation of Regulatory T Cells (Tregs)
MSCs promote the expansion and activity of Tregs, which:
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Suppress other T lymphocytes (including Th1, Th17);
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Reduce inflammation;
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Participate in maintaining immune tolerance.
Effects in Practice
After MSC administration in psoriasis or other autoimmune disease models, the following is observed:
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Decrease in the number of activated CD4+ and CD8+ T cells;
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Reduction in pro-inflammatory cytokine levels;
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Increase in Tregs and restoration of immune balance.
MSCs act as “peacemakers” in the immune system by suppressing aggressive T cell responses and stimulating regulatory pathways. This makes them a powerful tool for combating autoimmune disorders — both theoretically and practically in experimental and clinical studies.
Overview of Clinical Results
1. Human Umbilical Cord-Derived Cells (UMSC):
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Phase 1/2a open-label study with 17 patients. During a 6-month follow-up, 47% of participants achieved PASI ≥ 40% improvement, and 17.6% experienced near-complete symptom resolution (PGA).
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No side effects were detected; an increase in Tregs and a reduction in Th17 cells were observed in responders.
2. Adipose-Derived MSCs (AD MSC):
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Case studies: in 12 patients, PASI 50 was maintained for nearly 10 months. In another dataset, 14 out of 17 participants retained PASI 50 for a year.
3. Systematic Reviews and Preclinical Studies:
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Reviews confirm the immunomodulatory potential of MSCs: reduced IL-17 and TNF-α levels, normalization of Treg/Th17 balance. Up to 60 clinical patients achieved marked remission.
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In 38 cases, inflammation suppression and slowed psoriasis progression were observed.
Conclusions
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Efficacy: Promising signs of response — in most UMSC patients, PASI ≥ 40% is achieved.
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Safety: No side effects; studies show good tolerance.
Stem cell therapy for psoriasis shows encouraging results: improvement in 50% of UMSC cases, long-term remissions in individual AD MSC cases, and high safety profile.