Founded in 2022, the Fassett laboratory studies the skin-centric and systemic neuroimmune biology of IL-31 in inflammatory diseases. 

We and others have shown that the cytokine interleukin 31 (IL-31) is a key molecule in these networks. During Dr. Fassett’s post-doctoral fellowship in K. Mark Ansel and Allan Basbaum’s laboratories at UCSF, she discovered that IL-31 signaling through sensory neurons modulates cutaneous T cell effector responses and monocyte-derived macrophage differentiation trajectories in chronic allergic dermatitis. 

IL-31 is produced by a very small number of immune cells and therapeutic blocking of its receptor results in impressive reduction of disease metrics in at least two very itchy chronic inflammatory skin conditions: atopic dermatitis and prurigo nodularis. Much of the tissue response to IL-31 may derive from its ability to activate a well-characterized population of sensory nerves that transmit itch. Curiously, little else is known about the pathways upstream and downstream of IL-31, how IL-31 impacts tissue inflammation (apart from itching-scratching induced injury), or how IL-31 regulates/is regulated by other factors produced in the milieu of chronically inflamed tissue. 

While Dr. Fassett’s foundational studies in the Ansel lab were performed in mouse models of chronic allergic dermatitis, we now pursue experiments in diverse mouse models of tissue inflammation because IL-31 is also associated with psoriasis vulgaris, familial lichen amyloidosis, and systemic sclerosis. Animal studies suggest it may also contribute to tissue pathology in allergic asthma. Given the understudied associations between IL-31 and human immune cell-mediated chronic diseases, development of mouse and human skin organoids that incorporate lymphocytes and sensory neurons is another team goal.