Julien SeneschalLaboratoire de Biothérapie des maladies génétiques inflammatoires et cancers (BMGIC) - Inserm / Université de Bordeaux
better understanding of vitiligo mechanisms and inflammatory pigmentary disorders
Mes recherches
I am professor of dermatology at the department of dermatology, university hospital of Bordeaux, National Reference Center for Rare Skin disorders and I am responsible for the management of skin inflammatory disorders including atopic dermatitis, psoriasis, vitiligo and skin symptoms associated with auto-immune diseases. After a post-doctoral fellowship at Harvard University, focusing my research on skin immunology and resident memory T cells under the direction of Prof. Thomas S. Kupper, I created the ATIP-Avenir immuno-dermatology team (INSERM U1035, University of Bordeaux) with the goal to better characterize the immune pathogenesis of vitiligo and other pigmentary disorders associated with inflammation. My research led to a better understanding of the immune mechanisms of vitiligo disease and highlighted the role of skin resident memory T cells in the disease. With the support of academic and industrial grants, my goal is to develop new therapies for vitiligo disease and other pigmentary disorders.
Mon projet ATIP-Avenir
Understanding the relationship between inflammation and epidermal melanocyte loss in vitiligo for the development of new targeted therapies.
Despite not being life threatening, vitiligo is often associated with a poor quality of life and can be considered as a near orphan disease because of the lack of effective therapies. Melanocyte loss is the pathological hallmark of vitiligo. Yet, whether such disappearance results from melanocyte death and/or detachment is still a matter of debate. Moreover, during flares of the disease, vitiligo is characterized by the presence of CD8+ resident memory T cells producing elevated levels of both IFNg and TNFa. Our ongoing research identifies an additional mechanism and shows that the combined activity of IFNg and TNFa induces melanocyte detachment in vitro and in vivo and this phenomenon is dependent of factors associated with melanocyte adhesion to the basal layer of the epidermis. These results could explain depigmentation associated with inflammation. Future experiments based on established methods (transcriptomic analyses, flow cytometry, in vitro models of reconstructed human pigmented epidermis and in vivo mouse models) will give a thorough analysis of this new mechanism to fully develop new strategies in vitiligo. Moreover, we will better connect inflammation and epidermal melanocyte response and function in vitiligo and other pigmentary disorders. Indeed, using a translational approach focusing on melanocytes and inflammation, my ambition is to move beyond conventional pigment cell biology towards a novel vision of the function of melanocytes in the skin physiology and immune-pathology to prevent their loss, as observed in vitiligo, and to decipher their precise function in skin chronic inflammatory disorders.