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T helper (Th)1, Th17 and Th2 imbalance in mesenchymal stem cells of adult patients with atopic dermatitis: at the origin of the problem
Author(s) -
Orciani M.,
Campanati A.,
Caffarini M.,
Ganzetti G.,
Consales V.,
Lucarini G.,
Offidani A.,
Di Primio R.
Publication year - 2017
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.15078
Subject(s) - mesenchymal stem cell , atopic dermatitis , immunology , chemokine , pathogenesis , tumor necrosis factor alpha , interleukin 17 , t helper cell , medicine , interleukin 23 , inflammation , interleukin , cancer research , biology , immune system , cytokine , t cell , pathology
Summary Background Atopic dermatitis ( AD ) is a chronic and inflammatory disease characterized by a marked imbalance of T helper (Th)2 vs. Th1/Th17 cells in the early phase of AD , whereas a mixed Th1/Th2 pattern of inflammation is usually found at the chronic stage. These features have not been extensively evaluated in undifferentiated skin cells of patients affected by AD . Objectives To evaluate the relative expression of 22 genes encoding Th1, Th2 and Th17 cytokines and the secretion of the corresponding proteins in cutaneous mesenchymal stem cells ( MSC s) isolated from skin of patients with AD ( AD ‐ MSC s) and their role in AD onset. Methods AD ‐ MSC s were isolated, characterized and profiled by polymerase chain reaction array and enzyme‐linked immunosorbent assay for the relative expression and secretion of cytokines involved in the Th1, Th2 and Th17 pathways. MSC s isolated from the skin of healthy people were used as controls (C‐ MSC s). Results AD ‐ MSC s showed an upregulation of many Th1/Th17 cytokines [interleukin ( IL )‐6, IL ‐8, IL ‐12, IL ‐13, IL ‐17A, IL ‐17F, transforming growth factor‐β, interferon‐γ], while Th2 chemokines ( IL ‐2, IL ‐4, IL ‐5, IL ‐23A) were downregulated in AD ‐ MSC s. Finally, some genes/proteins ( CCL 1, IL ‐17C, tumour necrosis factor‐α) did not show variations between C‐ MSC s and AD ‐ MSC s. Conclusions The profile of MSC s obtained from patients with chronic AD retraces the Th1/Th17 cell environment observed in differentiated cells of chronic AD . This evidence could open a new scenario in the pathogenesis of AD , according to which the inflammatory process may involve MSC s early on.