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Characterization of CD 45 RO + memory T lymphocytes in keloid disease
Author(s) -
Chen Z.,
Zhou L.,
Won T.,
Gao Z.,
Wu X.,
Lu L.
Publication year - 2018
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/bjd.16173
Subject(s) - keloid , cytotoxic t cell , scars , cd8 , il 2 receptor , immunology , cytokine , foxp3 , medicine , t lymphocyte , interleukin , t cell , immune system , pathology , biology , in vitro , biochemistry
Summary 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 CD 45 RO + 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 CD 8 + 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 − CD 8 − memory T cells, with lower TNF ‐α production and enhanced interferon‐γ production. Furthermore, FOXP 3 + CD 8 − memory T cells in keloid scars were abnormal, including showing reduced CD 25 and cytotoxic T‐lymphocyte‐associated antigen 4 expression and interleukin‐10 production. In addition, a significant decrease in the number of CD 4 + CD 25 high FOXP 3 + regulatory T cells was identified in patients with multiple keloid scars. We also found that there was significantly increased infiltration of CD 103 + CD 8 + memory T cells in keloid scars. Conclusions Our findings preliminarily elucidate the abnormalities of CD 45 RO + memory T cells in keloid scars and provide early evidence that a disrupted T‐cell response contributes to the progression of KD .