The Role of IL-17 Cytokines in Psoriasis

Mosca, Megan; Hong, Julie; Hadeler, Edward; Hakimi, Marwa; Liao, Wilson; Bhutani, Tina

doi:10.2147/itt.s240891

Cited by 45 publications

(29 citation statements)

References 74 publications

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“…Therefore, a greater understanding of how Th17 cells and IL-17 are involved in the pathogenesis of SLE will help determine whether IL-17 is a promising therapeutic target. Novel biologic agent targeting directed toward IL-17 (secukinumab, ixekizumab, bimekizumab) and IL-17R (brodalumab) are approved for the treatment of psoriasis in the United States (38). A phase III, randomized, double-blind, placebo-controlled, 2-year study to evaluate the efficacy and safety of secukinumab in combination with standard therapy in patients with SLE with active nephritis (NCT04181762) is currently ongoing.…”

Section: Discussionmentioning

confidence: 99%

IL-17–producing follicular Th cells enhance plasma cell differentiation in lupus-prone mice

Kim¹,

Lee²,

Tian³

et al. 2022

JCI Insight

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Section: Discussionmentioning

confidence: 99%

IL-17–producing follicular Th cells enhance plasma cell differentiation in lupus-prone mice

Kim¹,

Lee²,

Tian³

et al. 2022

JCI Insight

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“…Finally, disease-specific cellular and molecular events in psoriasis are directly linked to the TNF–IL-23–Th17 inflammatory pathway [ 41 ]. The IL-17 cytokine family consists of six members (IL-17A, IL-17B, IL-17C, IL-17D, IL-17E and IL17F), with IL-17A and IL-17F being primarily associated with clinically relevant signaling in psoriasis, acting through the same receptor, but with varying potencies [ 42 ]. The biological effects of IL-17A are greater than those exerted by IL-17F, while the IL-17A/IL-17F heterodimer has an intermediate effect.…”

Section: Immunopathogenesis Of Psoriasis Vulgarismentioning

confidence: 99%

Oxidative Stress Induced by High Salt Diet—Possible Implications for Development and Clinical Manifestation of Cutaneous Inflammation and Endothelial Dysfunction in Psoriasis vulgaris

et al. 2022

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Although oxidative stress is recognized as an important effector mechanism of the immune system, uncontrolled formation of reactive oxygen and nitrogen species promotes excessive tissue damage and leads to disease development. In view of this, increased dietary salt intake has been found to damage redox systems in the vessel wall, resulting in endothelial dysfunction associated with NO uncoupling, inflammation, vascular wall remodeling and, eventually, atherosclerosis. Several studies have reported increased systemic oxidative stress accompanied by reduced antioxidant capacity following a high salt diet. In addition, vigorous ionic effects on the immune mechanisms, such as (trans)differentiation of T lymphocytes are emerging, which together with the evidence of NaCl accumulation in certain tissues warrants a re-examination of the data derived from in vitro research, in which the ionic influence was excluded. Psoriasis vulgaris (PV), as a primarily Th17-driven inflammatory skin disease with proven inflammation-induced accumulation of sodium chloride in the skin, merits our interest in the role of oxidative stress in the pathogenesis of PV, as well as in the possible beneficial effects that could be achieved through modulation of dietary salt intake and antioxidant supplementation.

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“…PS is strongly associated with dysfunctional helper T cells (Th1, Th17, Th22, and Treg) and is characterized by sharply delineated scaly erythematous plaques. In plaque PS, the intricate inflammatory cascade mediated by the IL-23/IL-17 pathway acts on keratinocytes, endothelial cells, and immune cells, thereby stimulating epidermal hyperplasia and the pro-inflammatory feed-forward circuit [ 71 ]. In addition, the function of Tregs, which play a fundamental role in immune homeostasis by suppressing immune responses, appears to be impaired in PS, which leads to an altered ratio of Th17 to Treg and exacerbation of the disease [ 72 ].…”

Section: Autophagy In Inflammatory Skin Diseasesmentioning

confidence: 99%

Autophagy: Guardian of Skin Barrier

et al. 2022

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Autophagy is a major degradation pathway that removes harmful intracellular substances to maintain homeostasis. Various stressors, such as starvation and oxidative stress, upregulate autophagy, and the dysregulation of autophagy is associated with various human diseases, including cancer and skin diseases. The skin is the first defense barrier against external environmental hazards such as invading pathogens, ultraviolet rays, chemical toxins, and heat. Although the skin is exposed to various stressors that can activate autophagy, the roles of autophagy in the skin have not yet been fully elucidated. Accumulating evidence suggests that autophagy is closely associated with pathogenesis and the treatment of immune-related skin diseases. In this study, we review how autophagy interacts with skin cells, including keratinocytes and immune cells, enabling them to successfully perform their protective functions by eliminating pathogens and maintaining skin homeostasis. Furthermore, we discuss the implications of autophagy in immune-related skin diseases, such as alopecia areata, psoriasis, and atopic dermatitis, and suggest that a combination of autophagy modulators with conventional therapies may be a better strategy for the treatment of these diseases.

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The Role of IL-17 Cytokines in Psoriasis

Cited by 45 publications

References 74 publications

IL-17–producing follicular Th cells enhance plasma cell differentiation in lupus-prone mice

IL-17–producing follicular Th cells enhance plasma cell differentiation in lupus-prone mice

Oxidative Stress Induced by High Salt Diet—Possible Implications for Development and Clinical Manifestation of Cutaneous Inflammation and Endothelial Dysfunction in Psoriasis vulgaris

Autophagy: Guardian of Skin Barrier

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