Cytokine modulation of atopic itch

Trier, Anna M.; Kim, Brian

doi:10.1016/j.coi.2018.05.005

Cited by 47 publications

(44 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…AD is predominantly associated with a type 2 immune response characterized by the elevated production of the cytokines IL-4, IL-5, IL-13, and IL-31. [7][8][9] In addition, epithelial cell-derived cytokines, such as IL-25, IL-33, and thymic stromal lymphopoietin, have been shown to directly promote these type 2 cytokine responses by acting on various effector immune cells. [10][11][12][13][14] Moreover, there is increasing support for the contribution of type 3 immune responses associated with the production of IL-17, IL-22, and IL-23 to AD pathogenesis.…”

mentioning

confidence: 99%

Treatment of atopic dermatitis with ruxolitinib cream (JAK1/JAK2 inhibitor) or triamcinolone cream

Kim

Howell

Sun

et al. 2020

Journal of Allergy and Clinical Immunology

154

156

View full text Add to dashboard Cite

show abstract

mentioning

confidence: 99%

Treatment of atopic dermatitis with ruxolitinib cream (JAK1/JAK2 inhibitor) or triamcinolone cream

Kim

Howell

Sun

et al. 2020

Journal of Allergy and Clinical Immunology

154

156

View full text Add to dashboard Cite

show abstract

“…Increased expression of epithelial cellederived and type 2 cytokines in the skin of patients with AD drive disease pathogenesis. 14,15 The expressions of key skin barrier proteins are impeded by inflammatory cytokines, which may further augment allergic sensitization and responses, impair protective innate immune responses, and trigger scratching, thereby damaging the skin and perpetuating the itch-scratch cycle. 14,[16][17][18][19] Janus kinases (JAKs) mediate type 2 and other cytokine signaling involved in the pathogenesis of AD.…”

mentioning

confidence: 99%

Effects of ruxolitinib cream on pruritus and quality of life in atopic dermatitis: Results from a phase 2, randomized, dose-ranging, vehicle- and active-controlled study

Kim

Sun

Papp

et al. 2020

Journal of the American Academy of Dermatology

View full text Add to dashboard Cite

Background: Atopic dermatitis (AD), a chronic, highly pruritic skin disorder, impairs quality of life (QoL). Janus kinase inhibitors suppress inflammatory and pruritus-associated cytokine signaling in AD. Objective: To report the effects of ruxolitinib (RUX) cream on itch and QoL in AD. Methods: A total of 307 adult patients with an Investigator's Global Assessment (score of 2 or 3) and 3% to 20% affected body surface area were randomly assigned for 8 weeks to receive double-blind treatment with RUX (1.5% twice daily, 1.5% once daily, 0.5% once daily, or 0.15% once daily), vehicle twice daily, or triamcinolone cream (0.1% twice daily for 4 weeks then vehicle for 4 weeks). Itch was measured by using the numerical rating scale, and patient QoL was assessed with Skindex-16. Results: Improvements in itch numerical rating scale and Skindex-16 were observed with RUX cream. Overall, 42.5% of patients who applied 1.5% RUX twice daily experienced minimal clinically important difference in itch within 36 hours of treatment (vehicle, 13.6%; P \ .01); near-maximal improvement was observed by week 4. Itch reduction was associated with improved QoL burden (Pearson correlation, 0.67; P \ .001). Significant improvements in Skindex-16 overall scores were noted at week 2. Limitations: Facial AD lesions were not treated.

show abstract

“…It is increasingly appreciated that the nervous system and immune system share common mediators. For example, Th2 cytokines, such as IL-4 and IL-13, figure prominently in the pathogenesis of allergy and asthma but also serve as neurotransmitters within the peripheral nervous system, where they mediate itch (115,116). Acetylcholine is a classic neurotransmitter of the CNS and the autonomic nervous system but is also secreted by a subpopulation of peripheral T cells (117,118).…”

Section: Workhop-identified Opportunitiesmentioning

confidence: 99%

Perfect timing: circadian rhythms, sleep, and immunity — an NIH workshop summary

et al. 2020

View full text Add to dashboard Cite

Recent discoveries demonstrate a critical role for circadian rhythms and sleep in immune system homeostasis. Both innate and adaptive immune responses-ranging from leukocyte mobilization, trafficking, and chemotaxis to cytokine release and T cell differentiation-are mediated in a time of day-dependent manner. The National Institutes of Health (NIH) recently sponsored an interdisciplinary workshop, "Sleep Insufficiency, Circadian Misalignment, and the Immune Response," to highlight new research linking sleep and circadian biology to immune function and to identify areas of high translational potential. This Review summarizes topics discussed and highlights immediate opportunities for delineating clinically relevant connections among biological rhythms, sleep, and immune regulation. Circadian rhythms are daily variations in behavior and biological activity that stem from an intrinsic ability of organisms to align themselves with the environmental 24-hour light/dark cycle. These rhythms originate from an internal biological clock that drives many aspects of human physiology, including the sleepwake cycle and daily variations in blood pressure, body temperature, and cortisol (1). A growing body of epidemiological evidence demonstrates an association between altering circadian timing through shift work or frequent time zone travel and increased rates of cardiovascular disorders, metabolic syndrome, and cancer (2-4). Clinical aspects of disease such as pain perception, asthma exacerbations, and myocardial infarctions are more common at certain times of day or night (5, 6). The discovery of the genetic basis for the circadian clock in the 1980s and 1990s has ushered in a new era in which long-appreciated circadian rhythms in physiology and clinical medicine are being reframed in terms of gene expression, metabolism, signal transduction, and cellular physiology (7). The translation of circadian discovery into strategies to improve the prevention and management of disease promises to be transformative, but at present, fundamental research is outpacing clinical application (Figure 1A). Much will depend on research identifying the critical mechanisms and targets to which circadian rhythm-based therapeutic strategies can be applied. An emerging example of exciting circadian discovery with potential clinical relevance is the intersection between circadian function and immune regulation (Figure 1B). The NIH recently sponsored a workshop entitled "Sleep Insufficiency, Circadian Misalignment, and the Immune Response" (May 16-17, 2019, Rockville, Maryland, USA). Its aim was to highlight basic and clinical advances linking sleep and circadian biology to immune dysfunction, thereby stimulating the application of circadian biology to translational medicine. The Workshop was cosponsored by four NIH institutes-the National Heart, Lung, and Blood Institute (NHLBI), National Institute on Aging (NIA), National Institute of Allergy and Infectious Diseases (NIAID), and National Institute on Alcohol Abuse and Alcoholism (NIAAA)-reflecting a...

show abstract

Cytokine modulation of atopic itch

Cited by 47 publications

References 45 publications

Treatment of atopic dermatitis with ruxolitinib cream (JAK1/JAK2 inhibitor) or triamcinolone cream

Treatment of atopic dermatitis with ruxolitinib cream (JAK1/JAK2 inhibitor) or triamcinolone cream

Effects of ruxolitinib cream on pruritus and quality of life in atopic dermatitis: Results from a phase 2, randomized, dose-ranging, vehicle- and active-controlled study

Perfect timing: circadian rhythms, sleep, and immunity — an NIH workshop summary

Contact Info

Product

Resources

About