16 search results for: mechanism of disease

What Went Wrong? How Dysregulated Type 2 Immunity Contributes to AD, PN, CSU, and BP
Dermatology
What Went Wrong? How Dysregulated Type 2 Immunity Contributes to AD, PN, CSU, and BP
expert video

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).

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Underlying Type 2 Inflammation Drives a Chronic Itch-Scratch Cycle in Atopic Dermatitis
Type 2 Inflammation
Underlying Type 2 Inflammation Drives a Chronic Itch-Scratch Cycle in Atopic Dermatitis
expert video

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.

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What Went Wrong? How Dysregulated Type 2 Immunity Contributes to AD, PN, CSU, and BP
Dermatology
What Went Wrong? How Dysregulated Type 2 Immunity Contributes to AD, PN, CSU, and BP
slide presentation

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).

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IL-4 Is the Primary Cytokine That Drives Th2 Cell Polarization and Amplifies Type 2 Inflammation
Type 2 Inflammation
IL-4 Is the Primary Cytokine That Drives Th2 Cell Polarization and Amplifies Type 2 Inflammation
expert video

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.

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