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Updated: Feb 17, 2026
Isolation, Culture, and Characterization of Primary Dermal Fibroblasts from Human Keloid Tissue
Published on: July 28, 2023
Characterization of CD45RO+ memory T lymphocytes in keloid disease
1Department of Plastic and Reconstructive Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Insights
Memory T cells show abnormalities in keloid disease (KD), with altered cytokine production and reduced regulatory T cells. This suggests a disrupted T-cell response contributes to keloid progression.
Area of Science:
- Immunology
- Dermatology
- Cell Biology
Background:
- Memory T cells are implicated in inflammatory skin disorders.
- The specific role of memory T cells in keloid disease (KD) is not well understood.
Purpose of the Study:
- To investigate the characteristics of CD45RO-positive (CD45RO+) memory T cells in keloid disease.
- To identify phenotypic and functional abnormalities of memory T cells in KD.
Main Methods:
- Isolation of primary cutaneous cells from keloid scars and normal skin.
- Isolation of peripheral blood mononuclear cells.
- Flow cytometry to analyze memory T cell phenotypes and functions in KD.
Main Results:
- The majority of T lymphocytes in keloid scars exhibited a memory phenotype.
- CD8-positive (CD8+) memory T cells in keloid scars showed reduced tumor necrosis factor-alpha (TNF-α) production.
- Abnormalities in Forkhead box P3 (FOXP3)-negative and FOXP3-positive CD8-negative memory T cells were observed, including altered cytokine production and marker expression.
- A significant decrease in CD4-positive (CD4+) CD25-high FOXP3-positive regulatory T cells was noted in patients with multiple keloid scars.
- Increased infiltration of CD103-positive CD8-positive memory T cells was found in keloid scars.
Conclusions:
- Preliminary elucidation of CD45RO+ memory T cell abnormalities in keloid scars.
- Provides early evidence for a disrupted T-cell response contributing to KD progression.
Background:
Memory T cells, a highly effective subset of T lymphocytes, have been reported to be involved in many inflammatory skin disorders. However, the potential role of memory T cells in keloid disease (KD) remains unclear.
Objectives:
Due to their important role in regulating inflammation, we investigated the characteristics of CD45RO+ memory T cells in KD.
Methods:
Primary cutaneous cells were isolated from keloid scars and normal skin by enzymic digestion. Peripheral blood mononuclear cells were isolated from a related blood sample, and flow cytometry was applied to identify the phenotypic and functional abnormalities of memory T cells in KD.
Results:
We observed that the majority of T lymphocytes in keloid scars had the memory phenotype, and a greater number of the CD8+ memory T cells in keloid scars produced lower levels of tumour necrosis factor (TNF)-α. This abnormal cytokine production was even more distinct in Forkhead box (FOX)P3- CD8- memory T cells, with lower TNF-α production and enhanced interferon-γ production. Furthermore, FOXP3+ CD8- memory T cells in keloid scars were abnormal, including showing reduced CD25 and cytotoxic T-lymphocyte-associated antigen 4 expression and interleukin-10 production. In addition, a significant decrease in the number of CD4+ CD25high FOXP3+ regulatory T cells was identified in patients with multiple keloid scars. We also found that there was significantly increased infiltration of CD103+ CD8+ memory T cells in keloid scars.
Conclusions:
Our findings preliminarily elucidate the abnormalities of CD45RO+ memory T cells in keloid scars and provide early evidence that a disrupted T-cell response contributes to the progression of KD.
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