42 search results for: mechanism of disease
CLCI in Atopic Dermatitis Infographic
This infographic highlights how uncontrolled moderate‑to‑severe atopic dermatitis (AD) can lead to Cumulative Life Course Impairment (CLCI) by contributing to ongoing physical, psychological, and social burdens such as itch and sleep loss, impaired bone growth and mental health challenges. It emphasizes the importance of early and effective disease control to help reduce long‑term impact on patients.
How Does Protective Type 2 Immunity Become Harmful Type 2 Inflammation?
In this video from the March 2025 ADVENT symposium in Orlando, Florida, Dr. Eric Simpson discusses how protective type 2 immunity can become dysregulated, leading to harmful type 2 inflammation. The associated inflammatory process can contribute to the pathophysiology of several dermatological diseases, including AD, PN, CSU, and BP.
From Protective Type 2 Immunity to Aberrant Type 2 Inflammation
In this soundbite video from the April 2025 ADVENT Forum in Lisbon, Portugal, Prof. Oscar Palomares explains how type 2 immunity evolved to protect against parasites, venoms, and toxins, and how its dysregulation can result in aberrant type 2 inflammation underlying multiple chronic inflammatory diseases.
Differential Effects of Dupilumab and JAK Inhibitors on CCL17 (TARC) in Patients With AD
In this soundbite video from the April 2025 ADVENT Forum in Lisbon, Portugal, Prof. Oscar Palomares compares the effects of biologics and JAK inhibitors on the biomarker CCL17 (TARC) in atopic dermatitis.
ERS 2024 | Pathophysiologic Mechanisms of Airway Remodeling in Severe Asthma
Professor Celeste Porsbjerg presents the pathophysiology and disease processes involved in airway remodeling in severe asthma.
KOL Video Interview – Dr Paula Luna
In this exclusive video interview, Dr Paula Luna discusses how disease modification can be defined in AD and how IgE may be used as a biomarker in AD.
Type 2 Cytokines Have Multiple Critical Roles in BP That Contribute to Inflammation and Itch
In this soundbite video from the April 2025 ADVENT Forum in Lisbon, Portugal, Dr. Eric Simpson outlines why early, targeted control of type 2 inflammation may modify the course of atopic dermatitis by addressing upstream drivers of barrier dysfunction, dysbiosis, and itch.
What Went Wrong? How Dysregulated Type 2 Immunity Contributes to AD, PN, CSU, and BP
This full video presentation of the March 2025 ADVENT cross-dermatology symposium, hosted in Orlando, Florida features Dr. Eric Simpson, Dr. Shawn Kwatra, Dr. Jason Hawkes and Dr. Victoria Werth. The faculty present the latest information around type 2 inflammation and its association with atopic dermatitis (AD), prurigo nodularis (PN), chronic spontaneous urticaria (CSU) and bullous pemphigoid (BP).
Underlying Type 2 Inflammation Drives a Chronic Itch-Scratch Cycle in Atopic Dermatitis
In this soundbite video from the April 2025 ADVENT Forum in Lisbon, Portugal, Dr. Brian Kim explains how underlying type 2 inflammation sustains the chronic itch-scratch cycle in atopic dermatitis, highlighting the interplay of barrier dysfunction, cytokine signaling, and neuronal activation.
What Went Wrong? How Dysregulated Type 2 Immunity Contributes to AD, PN, CSU, and BP
This is the full presentation of the March 2025 ADVENT cross-dermatology symposium, hosted in Orlando, Florida, presenting the latest information around type 2 inflammation and its association with atopic dermatitis (AD), prurigo nodularis (PN), chronic spontaneous urticaria (CSU) and bullous pemphigoid (BP).
How Does Protective Type 2 Immunity Become Harmful Type 2 Inflammation?
In this video soundbite from the March 2025 ADVENT symposium in Orlando, Florida, Dr. Eric Simpson explains how protective type 2 immunity can become dysregulated, leading to harmful type 2 inflammation.
IL-4 Is the Primary Cytokine That Drives Th2 Cell Polarization and Amplifies Type 2 Inflammation
In this soundbite video from the April 2025 ADVENT Forum in Lisbon, Portugal, Prof Oscar Palomares describes how IL-4 is the key cytokine involved in the initiation and perpetuation of Th2 cell responses and type 2 inflammation.
