“…This result indicates that dupilumab can impair the protective role for IL-4/IL-13 in Th17-associated enthesitis. Consistently, in our case and a previous five cases who were examined by ultrasound, 1,3,4 features of enthesitis were detected. Among the five cases whose courses after diagnosis were reported, three stopped dupilumab therapy and two continued the therapy with additional oral celecoxib like our case.…”
Section: Arthritis and Enthesitis During Dupilumab Therapy Completely Remitted By Celecoxibsupporting
confidence: 91%
“…There have been six reported cases with arthritis or enthesitis whose onset was within 16 weeks after initiation of dupilumab therapy for AD (Table S1). [1][2][3][4] Bridegwood et al 4 found that IL-4/IL-13 suppressed IL-23 expression from digested enthesis tissue treated with lipopolysaccharide. This result indicates that dupilumab can impair the protective role for IL-4/IL-13 in Th17-associated enthesitis.…”
Section: Arthritis and Enthesitis During Dupilumab Therapy Completely Remitted By Celecoxibmentioning
“…This result indicates that dupilumab can impair the protective role for IL-4/IL-13 in Th17-associated enthesitis. Consistently, in our case and a previous five cases who were examined by ultrasound, 1,3,4 features of enthesitis were detected. Among the five cases whose courses after diagnosis were reported, three stopped dupilumab therapy and two continued the therapy with additional oral celecoxib like our case.…”
Section: Arthritis and Enthesitis During Dupilumab Therapy Completely Remitted By Celecoxibsupporting
confidence: 91%
“…There have been six reported cases with arthritis or enthesitis whose onset was within 16 weeks after initiation of dupilumab therapy for AD (Table S1). [1][2][3][4] Bridegwood et al 4 found that IL-4/IL-13 suppressed IL-23 expression from digested enthesis tissue treated with lipopolysaccharide. This result indicates that dupilumab can impair the protective role for IL-4/IL-13 in Th17-associated enthesitis.…”
Section: Arthritis and Enthesitis During Dupilumab Therapy Completely Remitted By Celecoxibmentioning
“…In line with previous reports, 1–6 we hypothesize that inhibiting the Th‐2 response with an IL‐4/IL‐13 signaling pathway blocking agent might result in a shift toward a Th‐1/Th‐17 phenotype. In predisposed patients, such a cytokine shift could then lead to an inflammatory cascade finally resulting in realization of psoriatic lesions.…”
“…77 The development of arthralgia and enthesitis, a characteristic feature of psoriatic arthritis, has also been reported after the use of dupilumab. 78 Furthermore, the administration of dupilumab worsens skin lesions in psoriasis. 79 It has also been reported that the administration of IL-4 improved psoriasis symptoms.…”
Section: Psoria S Is a S A Counterpart To Atopi C Dermatitismentioning
Psoriasis is a complex chronic inflammatory skin disease caused by the dynamic interplay between multiple genetic risk foci, environmental risk factors, and excessive immunological abnormalities. Psoriasis affects approximately 2% of the population worldwide, and dramatic advances have been achieved in the understanding and treatment options for psoriasis. Recent progress in biological therapies has revealed the fundamental roles of tumor necrosis factor‐α, interleukin (IL)‐23p19, and the IL‐17A axis together with skin‐resident immune cells and major signal transduction pathways in the pathogenesis of psoriasis. In addition to IL‐17‐producing T helper17 cells, innate lymphoid cell (ILC)3 induces psoriasis rashes directly without T‐cell/antigen interaction in response to the released antimicrobial peptides from activated keratinocytes and inflammatory cytokines. ILC3 typically expresses retinoic acid receptor‐related orphan receptor gamma t in the nucleus, matures in the presence of IL‐7 and IL‐23, and produces IL‐17 and IL‐22. The number of ILC3s is increased in the blood, psoriasis rash, and even in nonrash areas of psoriatic skin. Psoriasis is significantly associated with cardiovascular disease, metabolic syndrome, and inflammatory disorders, particularly the severe type. The similarity of enterobacteria in the psoriasis gut to that in diabetic patients may be related to its pathogenesis. In the current review, we focus on the pathophysiology of psoriasis in the accelerated immunological inflammatory loop, danger signal from keratinocytes, and cytokines, particularly IL‐17 and IL‐23p19. In addition, pathophysiological speculation with regard to morphology has been supplemented. Finally, the differences and similarities between psoriasis and atopic dermatitis are discussed.
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