Identification of a Th2‐ and Th17‐skewed immune phenotype in chronic urticaria with Th22 reduction dependent on autoimmunity and thyroid disease markers

Moy, Andrea P.; Murali, Mandakolathur R.; Nazarian, Rosalynn M.

doi:10.1111/cup.12673

Cited by 25 publications

(19 citation statements)

References 54 publications

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“…As it is the MC T subtype of mast cells that is particularly associated with allergic disease, this would support an allergic mechanism for CSU. In contrast, other studies found no difference between mast cell numbers in the skin of chronic urticaria patients and healthy individuals …”

Section: Mast Cell Location and Changes In Number In Chronic Urticariamentioning

confidence: 70%

The role and relevance of mast cells in urticaria

Church

Kolkhir

Metz

et al. 2018

Immunological Reviews

223

198

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This review presents evidence that the skin mast cell, in particular the MC subtype, is the primary effector cell in urticaria. Mast cells are located in the upper dermis, the ideal situation for wheal formation and sensory nerve stimulation. Increased numbers of mast cells are found in both lesional and non-lesional skin in CSU and inducible urticaria. Mast cell degranulation in the area of wheals has been demonstrated repeatedly by light and electron microscopy. Histamine, PGD and tryptase are found in the venous blood draining wheal formation. The last 2 are specific for mast cells rather than basophils. Mast cell reactivity is increased in active urticaria by local inflammatory cytokines and neuropeptides. Mast cell cytokines and neuropeptides, particularly nerve growth factor, induce a Th2 type inflammation that is particularly obvious at the sites of whealing. In conclusion, autoimmunity, either of Type 1 viz. IgE antibodies to local autoallergens, or Type 2b, viz. IgG autoantibodies to IgE or its receptor, are considered to be the most frequent causes of CSU. In both cases, the mast cell is likely to be the axial cell in producing the wheals.

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Section: Mast Cell Location and Changes In Number In Chronic Urticariamentioning

confidence: 70%

The role and relevance of mast cells in urticaria

Church

Kolkhir

Metz

et al. 2018

Immunological Reviews

223

198

View full text Add to dashboard Cite

show abstract

“…CD3+ T cells and dual‐labelled cells (e.g. cells with both cytoplasmic CD4+ staining and nuclear T‐bet+ staining) were counted in five consecutive high power fields (HPFs) at × 400 magnification, in a blinded, independent fashion by two of the authors (APM and RMN), as previously described . The number of Th1, Th2, Th17 and Th22 cells as a percentage of CD3+ T cells were calculated.…”

Section: Methodsmentioning

confidence: 99%

T-helper immune phenotype may underlie ‘paradoxical’ tumour necrosis factor-α inhibitor therapy-related psoriasiform dermatitis

et al. 2017

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SummaryBackground. Therapeutics targeting tumour necrosis factor (TNF)-a are effective for psoriasis; however, in patients treated for other disorders, psoriasis may worsen and psoriasiform dermatitis (PsoD) may arise. T helper (Th) cytokines in psoriasis upregulate keratin (K)17, which modulates TNF-a transduction, leading to vascular adhesion molecule upregulation and lymphocytic extravasation. Aim. We investigated Th phenotype and expression of K17, intercellular adhesion molecule (ICAM)-1 and vascular adhesion molecule (VCAM)-1 in psoriasis and anti-TNF-a-related PsoD. Methods. Skin biopsies from patients with psoriasis unresponsive to TNF-a inhibitor therapy (n = 11), PsoD-related to TNF-a inhibition (n = 9), untreated psoriasis (n = 9) or atopic dermatitis (AD; n = 9) were immunohistochemically analysed for Th1, Th2, Th17 and Th22. Expression of K17, ICAM-1 and VCAM-1 was also examined. Results. Anti-TNF-a-unresponsive psoriasis and anti-TNF-a-related PsoD showed decreased Th1 : Th2 raio and increased Th17 : Th1 ratio compared with untreated psoriasis. Anti-TNF-a-unresponsive psoriasis had significantly fewer Th1 (4% vs. 12%) and more Th17 (51% vs. 20%) cells than untreated psoriasis. No difference in Th22 cells was identified. K17 was present in all cases of untreated psoriasis and anti-TNF-a-related PsoD, 91% of anti-TNF-a-unresponsive psoriasis, and only 22% of AD. VCAM-1 and ICAM-1 in anti-TNF-a-related PsoD was akin to untreated psoriasis, but decreased in anti-TNF-a-unresponsive psoriasis. Conclusions. These findings further the current understanding of the anti-TNF-arelated psoriasiform phenotype and support a rationale for therapeutic targeting of interleukin-17 and TNF-a in combination.

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“…Th17 cells show both inhibitory and stimulatory effects on antibody production by mast cells (6). Of particular relevance to the current study are the recent findings revealing that Th2/ Th17 cytokines, transcription factors and Th2 chemo kines are upregulated or elevated in CSU patients' skin lesions, plasma and serum, respectively (7)(8)(9)(10). Accordingly, Th2 and Th17 pathways may be involved in the pathogenesis of CSU, and CCL17 and IL-17 can serve as serum markers of Th2 and Th17 inflammation, respectively.…”

mentioning

confidence: 63%

Serum miR-125a-5p and CCL17 Upregulated in Chronic Spontaneous Urticaria and Correlated with Treatment Response

Zhang¹,

Qi²,

Yang³

et al. 2019

Acta Derm Venerol

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Currently, there exist no generally accepted objective biomarkers for chronic spontaneous urticaria. Therefore, the identification of new categories of biomarkers for chronic spontaneous urticaria are urgently needed. To the best of our knowledge, no published information is available regarding serum miRNA as related to chronic spontaneous urticaria. In this study, we provide new and important findings which show that serum expression of miR-125a-5p and CCL17 are significantly upregulated in patients with active chronic spontaneous urticaria and significantly decreased in the remission phase. Moreover, a further upregulation in serum miR-125a-5p expression was observed in refractory chronic spontaneous urticaria cases. These results highlight the significance of miR-125a-5p and CCL17 as potential serum biomarkers for chronic spontaneous urticaria. Chronic spontaneous urticaria (CSU) is a common skin disorder associated with autoimmunity. Micro RNAs (miRNAs) are endogenous noncoding RNA mo lecules reported to be potential biomarkers for some autoimmune diseases. In this study, we investigated the association of miRNAs with CSU. A quantitative PCR (qPCR)based array was generated from sera as obtained from 20 active CSU patients and 20 healthy controls. Upregulated or downregulated miRNAs were validated by reverse transcription qPCR in sera from 59 active CSU patients and 58 healthy controls. The ex pression of miR-125a-5p was significantly upregulated in CSU sera and serum levels of CCL17 were also signi ficantly increased in CSU patients. Serum miR-125a-5p expressions were found to be further upregulated in refractory CSU cases (n = 10). In 12 CSU patients in remission, serum miR125a5p expression and CCL17 levels were significantly decreased as compared with that obtained in active phase patients. These results indicated that miR125a5p and CCL17 can serve as potential serum biomarkers for CSU.

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Identification of a Th2‐ and Th17‐skewed immune phenotype in chronic urticaria with Th22 reduction dependent on autoimmunity and thyroid disease markers

Abstract: These findings provide novel insight into the role of Th2 and Th17 in chronic urticaria pathophysiology and may impact therapy.

Cited by 25 publications

References 54 publications

The role and relevance of mast cells in urticaria

The role and relevance of mast cells in urticaria

T-helper immune phenotype may underlie ‘paradoxical’ tumour necrosis factor-α inhibitor therapy-related psoriasiform dermatitis

Serum miR-125a-5p and CCL17 Upregulated in Chronic Spontaneous Urticaria and Correlated with Treatment Response

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