The British journal of dermatology · 2018
Characterization of CD45RO+ memory T lymphocytes in keloid disease.
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Chen Z, Zhou L, Won T, Gao Z, Wu X, Lu L
Аннотация
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.
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.