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Immune cells in the blood of people with vitiligo
Publication year - 2020
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/bjd.19519
Subject(s) - vitiligo , immune system , disease , immunology , medicine , dermatology , pathology
Vitiligo is a disease in which white patches appear on the skin due to loss of pigment cells (melanocytes). It is an “auto‐immune disease” caused by the body’s immune system targeting melanocytes, but we don’t entirely understand how this works. We know it involves white blood cells called T‐lymphocytes and that the balance between “helper” and “cytotoxic” T‐lymphocytes is important. We also know that two particular blood chemicals (“cytokines”), interferon‐y (IFN‐y) and tumour necrosis factor‐a (TNF‐a), control that balance. However, these cells and cytokines occur in other conditions too, and in healthy people, so we need much more detail in order to develop targeted treatments. In this study, researchers in France analysed immune cells from the blood of 60 people with vitiligo, 25 people with psoriasis (another auto‐immune disease) and 28 healthy people. They found reduced numbers of certain populations of T‐cells in both vitiligo and psoriasis; they had previously reported increased numbers of these cell subsets in the skin around vitiligo patches, suggesting that these cells migrate from blood into the skin. Surprisingly, they found no differences between people with actively spreading vitiligo and those with stable (not spreading) patches. Also, cytokine production was the same in vitiligo, psoriasis and healthy controls. These findings support the idea that drugs targeting specific T‐cell subsets in the blood might prevent flares and progression of vitiligo. However, as the accompanying commentary by TR Matos points out, more work is needed to discover exactly which blood cells migrate to the skin and damage melanocytes. Linked Article: Martins et al. Br J Dermatol 2020; 183: 899–908.