دورية أكاديمية
T-helper immune phenotype may underlie 'paradoxical' tumour necrosis factor-α inhibitor therapy-related psoriasiform dermatitis.
| العنوان: | T-helper immune phenotype may underlie 'paradoxical' tumour necrosis factor-α inhibitor therapy-related psoriasiform dermatitis. |
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| المؤلفون: | Moy, A. P., Murali, M., Kroshinsky, D., Horn, T. D., Nazarian, R. M. |
| المصدر: | Clinical & Experimental Dermatology; Jan2018, Vol. 43 Issue 1, p19-26, 8p, 2 Diagrams, 1 Chart |
| مصطلحات موضوعية: | TUMOR necrosis factors, SKIN inflammation, ATOPIC dermatitis, SKIN biopsy, TH1 cells |
| مستخلص: | Background 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. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: | Complementary Index |
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