Aims: Vitiligo is an epidermal disorder hallmarked by destruction of melanocytes due to oxidative stress and the subsequent activation of both innate and adaptive autoimmunity. As progeny of Schwann cells, melanocytes have remarkable biological similarities to both glial and neuronal cells. Neurotrophins are known to regulate proliferation, survival, apoptosis, differentiation and inflammation in mammalian skin, including melanocytes. As such a neuroendocrine theory of vitiligo has been postulated. TkrB, tropomyosin-related kinase receptor type B, a regulator of cell survival and growth, has been previously identified to be expressed in melanocytes. We sought to explore the role of brain derived neurotrophic factor (BDNF), the canonical high affinity ligand for the TrkB receptor in vitiligo.
Methods: A systematic search of MEDLINE, EMBASE and Cochrane was performed to identify published cases of vitiligo and brain derived neurotrophic factor. BDNF in vitiligo lesions and perilesional vitiligo skin was assessed using immunofluorescence of FFPE sections.
Results: Vitiligo patients have lower extracellular levels of BDNF, with a standardised mean difference (95% CI) of -0.92 (-1.79 to -0.06). BDNF is abundant in human epidermis, predominantly in squamous keratinocytes, which demonstrate cytoplasmic staining. Lesional vitiligo skin has lower abundance of BDNF compared to perilesional skin on immunofluorescence.
Conclusions: Vitiligo lesions are depleted of BDNF, which may impair TkrB signaling, diminishing melanocyte survival. The functional role of BDNF signaling in melanocytes should be further explored to establish its role in melanocyte survival and vitiligo pathogenesis.