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- W2940378003 abstract "Alopecia areata (AA) is a common autoimmune disease, causing patchy hair loss that can progress to involve the entire scalp (totalis) or body (universalis). CD8+NKG2D+ T cells dominate hair follicle pathogenesis, but the specific mechanisms driving hair loss are not fully understood. To provide a detailed insight into the systemic cytokine signature associated with AA, and to assess the association between cytokines and depression. We conducted multiplex analysis of plasma cytokines from patients with AA, patients with psoriatic arthritis (PsA) and healthy controls. We used the Hospital Anxiety and Depression Scale (HADS) to assess the occurrence of depression and anxiety in our cohort. Our analysis identified a systemic inflammatory signature associated with AA, characterized by elevated levels of interleukin (IL)‐17A, IL‐17F, IL‐21 and IL‐23 indicative of a type 17 immune response. Circulating levels of the type 2 cytokines IL‐33, IL‐31 and IL‐17E (IL‐25) were also significantly increased in AA. In comparison with PsA, AA was associated with higher levels of IL‐17F, IL‐17E and IL‐23. We hypothesized that circulating inflammatory cytokines may contribute to wider comorbidities associated with AA. Our assessment of psychiatric comorbidity in AA using HADS scores showed that 18% and 51% of people with AA experienced symptoms of depression and anxiety, respectively. Using linear regression modelling, we identified that levels of IL‐22 and IL‐17E are positively and significantly associated with depression. Our data highlight changes in both type 17 and type 2 cytokines among people with AA, suggesting that complex systemic cytokine profiles may contribute both to the pathogenesis of AA and to the associated depression. What's already known about this topic? NKG2D+CD8+ T cells cause hair loss in alopecia areata (AA) but the immunological mechanisms underlying the disease are not fully understood. AA is associated with changes in levels of interleukin (IL)‐6, tumour necrosis factor‐α, IL‐1β and type 17 cytokines. Psychiatric comorbidity is common among people with AA. What does this study add? People with AA have increased plasma levels of the type 2 cytokines IL‐33, IL‐31 and IL‐17E (IL‐25), in addition to the type 17 cytokines IL‐17A, IL‐21, IL‐23 and IL‐17F. Levels of IL‐17E and IL‐22 positively predict depression score. What is the translational message? AA is associated with increased levels of multiple inflammatory cytokines, implicating both type 17‐ and type 2 immune pathways. Our data indicate that therapeutic strategies for treating AA may need to address the underlying type 17‐ and type 2 immune dysregulation, rather than focusing narrowly on the CD8+ T‐cell response. An immunological mechanism might contribute directly to the depression observed in people with AA." @default.
- W2940378003 created "2019-04-25" @default.
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- W2940378003 date "2019-07-17" @default.
- W2940378003 modified "2023-10-10" @default.
- W2940378003 title "Alopecia areata is characterized by dysregulation in systemic type 17 and type 2 cytokines, which may contribute to disease‐associated psychological morbidity" @default.
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- W2940378003 cites W1651325956 @default.
- W2940378003 cites W1904080427 @default.
- W2940378003 cites W1941472782 @default.
- W2940378003 cites W1966059955 @default.
- W2940378003 cites W1977333143 @default.
- W2940378003 cites W1985438873 @default.
- W2940378003 cites W1988280501 @default.
- W2940378003 cites W1997825162 @default.
- W2940378003 cites W1998000193 @default.
- W2940378003 cites W1999468608 @default.
- W2940378003 cites W2014750930 @default.
- W2940378003 cites W2019475856 @default.
- W2940378003 cites W2031487819 @default.
- W2940378003 cites W2034040607 @default.
- W2940378003 cites W2041959340 @default.
- W2940378003 cites W2046572145 @default.
- W2940378003 cites W2047003778 @default.
- W2940378003 cites W2048162737 @default.
- W2940378003 cites W2049804077 @default.
- W2940378003 cites W2060050678 @default.
- W2940378003 cites W2068080380 @default.
- W2940378003 cites W2068556120 @default.
- W2940378003 cites W2073957455 @default.
- W2940378003 cites W2076896224 @default.
- W2940378003 cites W2078873723 @default.
- W2940378003 cites W2091259554 @default.
- W2940378003 cites W2091766197 @default.
- W2940378003 cites W2095828085 @default.
- W2940378003 cites W2103825953 @default.
- W2940378003 cites W2127542434 @default.
- W2940378003 cites W2139998911 @default.
- W2940378003 cites W2144625497 @default.
- W2940378003 cites W2166281097 @default.
- W2940378003 cites W2170558579 @default.
- W2940378003 cites W2199733448 @default.
- W2940378003 cites W2201607793 @default.
- W2940378003 cites W2270215994 @default.
- W2940378003 cites W2317492969 @default.
- W2940378003 cites W2339275879 @default.
- W2940378003 cites W2425787389 @default.
- W2940378003 cites W2515031566 @default.
- W2940378003 cites W2521310721 @default.
- W2940378003 cites W2525291061 @default.
- W2940378003 cites W2548580472 @default.
- W2940378003 cites W2617690685 @default.
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- W2940378003 cites W2790698850 @default.
- W2940378003 cites W2807318413 @default.
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- W2940378003 cites W2897965012 @default.
- W2940378003 cites W4211054359 @default.
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- W2940378003 doi "https://doi.org/10.1111/bjd.18008" @default.
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