I. C. Le Poole

TL;DR: During the 2011 International Pigment Cell Conference (IPCC), the Vitiligo European Taskforce (VETF) convened a consensus conference on issues of global importance for vitiligo clinical research, agreeing that disease stability be best assessed based on the stability of individual lesions rather than the overall stability of the disease as the latter is difficult to define precisely and reliably.

TL;DR: Results presented in this study are very suggestive of involvement of local immune reactivity in melanocyte destruction within perilesional epidermis, and inflammation is accompanied by increased tenascin content.

TL;DR: Several theories on vitiligo etiopathogenesis have been combined to formulate a convergence theory, which stales that stress, accumulation of toxic compounds, infection, autoimmunity, mutations, altered cellular environment and impaired melanocyte migration and or proliferation can all contribute to vitiligosis in varying proportions.

TL;DR: As a more effective therapy for this common, often disfiguring pigmentary disorder is direly needed, it must strive harder to settle the pathogenesis debate definitively – on the basis of sound experimental evidence, rather than by a war of dogmatic theories.

TL;DR: It is demonstrated that cultured normal human skin melanocytes can present peptide Ag, and process and present the mycobacterial HSP65 kDa protein and whole Mycobacterium leprae sonicate to CD4+ cytotoxic proliferative T cell clones in an Ag-specific and HLA-class II-restricted manner.