Explore the
Mechanism of Action
This image is for illustrative purposes only.
This image is for illustrative purposes only.
IFN-γ mediated JAK-STAT signaling is thought to drive an inflammatory cycle, creating a hostile environment in which CD8+ T-cells target and destroy melanocytes.⁵ Autoimmune IFN-γ producing cytotoxic T lymphocytes are thought to be directly responsible for melanocyte destruction in human vitiligo.⁶
Adapted from ref. 5
Intrinsic and/or extrinsic factors induce the cellular stress response in melanocytes, which then activates innate immunity within the skin to trigger the initial inflammation that leads to autoimmunity.⁵
IFN-γ secreted by CD8+T cells.⁵
Under IFN-γ activation, JAK-STAT pathway triggers chemokines CXCL9 and CXCL10 in keratinocytes.⁵
Chemokines attract more CD8+T cells, which destroy melanocytes and lead to depigmentation.⁵
Ruxolitinib cream has been found to have physicochemical properties suitable for topical delivery through the skin of patients with inflammatory skin diseases.⁷
Adapted from ref. 8
In addition to Ruxolitinib’s anti-IFN-γ effect, it also seems to activate the hair follicle melanocyte stem cell.⁹
CD: Cluster of Differentiation; CXCL: C-X-C motif chemokine ligand; IFN-ɣ: Interferon gamma; JAK: Janus kinase; STAT: Signal Transducer and Activator of Transcription.
Are you a healthcare professional practising in Hong Kong and Macau?