Jason Ezra Hawkes, MD, MS, FAAD, board-certified dermatologist and associate professor of dermatology at the University of California Davis in Sacramento, explained the utility of type 2 inflammation pathways and the microbiome in understanding the immune dysregulation associated with atopic dermatitis (AD).
Type 2 inflammatory pathways are key in the evaluation of atopic dermatitis (AD), with other factors such as the microbiome and presence of comorbidities also relevant, said Jason Ezra Hawkes, MD, MS, FAAD, board-certified dermatologist and associate professor of Dermatology at the University of California Davis in Sacramento
Can you discuss key pathophysiological differences between AD and other immune-regulated skin conditions, and how these factors play into screening for the disease?
When we think about the immunology of atopic dermatitis compared to other skin conditions, we're really kind of focusing on the central T helper 2 [Th2] or type 2 inflammation pathways. So, IL [interleukin]-4 and IL-13 have been shown to be really central to the skin condition, but there's other factors that I think make AD a little bit different from some of the other conditions.
So, we definitely see a skin barrier dysfunction, or disruption of the skin barrier, and that's definitely a function of the immune dysregulation that occurs. That also leads to perpetuation of changes in the microbiome. These patients are quite sensitive to skin infection. So, I think of those as being really central, the Th2 response to skin barrier disruption, and then this change in the microbiome that happens over time.
The other thing that helps me evaluate these patients is we start to see this overlap between other comorbid conditions or other atopic conditions. So, seasonal allergies, food allergies, asthma, hypersensitivity, sebborheic dermatitis, or dandruff—these are really common things that we see in these patients that also sort of stretch out into family members.