T-helper immune phenotype may underlie ‘paradoxical’ tumour necrosis factor-α inhibitor therapy-related psoriasiform dermatitis
| Autor: | T. D. Horn, Rosalynn M. Nazarian, Andrea P. Moy, Daniela Kroshinsky, Mandakolathur R. Murali |
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| Rok vydání: | 2017 |
| Předmět: |
Adult
Male Necrosis Biopsy Drug Resistance Dermatitis Dermatology 030207 dermatology & venereal diseases 03 medical and health sciences 0302 clinical medicine Psoriasis medicine Humans Psoriasiform Dermatitis Aged Skin Aged 80 and over medicine.diagnostic_test Tumor Necrosis Factor-alpha business.industry Interleukin-17 T-Lymphocytes Helper-Inducer Atopic dermatitis Middle Aged Intercellular adhesion molecule medicine.disease Extravasation Phenotype 030220 oncology & carcinogenesis Immunology Female Tumor necrosis factor alpha medicine.symptom business |
| Zdroj: | Clinical and Experimental Dermatology. 43:19-26 |
| ISSN: | 0307-6938 |
| Popis: | SummaryBackground Therapeutics targeting tumour necrosis factor (TNF)-α 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-α 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-α-related PsoD. Methods Skin biopsies from patients with psoriasis unresponsive to TNF-α inhibitor therapy (n = 11), PsoD-related to TNF-α 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-α-unresponsive psoriasis and anti-TNF-α-related PsoD showed decreased Th1 : Th2 raio and increased Th17 : Th1 ratio compared with untreated psoriasis. Anti-TNF-α-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-α-related PsoD, 91% of anti-TNF-α-unresponsive psoriasis, and only 22% of AD. VCAM-1 and ICAM-1 in anti-TNF-α-related PsoD was akin to untreated psoriasis, but decreased in anti-TNF-α-unresponsive psoriasis. Conclusions These findings further the current understanding of the anti-TNF-α-related psoriasiform phenotype and support a rationale for therapeutic targeting of interleukin-17 and TNF-α in combination. |
| Databáze: | OpenAIRE |
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