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We read with interest the recent paper by Facco et al which showed that Th17 cells are present in blood, bronchoalveolar lavage (BAL) and lung tissue from people with sarcoidosis. The authors conclude that Th17 cells are involved in the pathogenesis of sarcoidosis as a multisystem disorder.1
Interestingly, the paper mentions expression of interleukin (IL)-17 protein by macrophages. Currently, a strong emphasis exists in the literature on the role of Th17 lymphocytes in the production of IL-17 in the lungs. However, Th17 cells are not the only source of IL-17 identified.2 IL-17 is also known to be produced by γδ and natural killer T cells.3 4 It has also been suggested that in human alcoholic liver disease, atherosclerosis and rodent models of lipopolysaccharide-induced airway inflammation IL-17 can be localised to neutrophils.5–7 Furthermore, we have recently demonstrated that IL-17 protein expression is raised in the lower airway of people with advanced cystic fibrosis lung disease.8 This IL-17 protein expression was immunolocalised to both neutrophils and mononuclear cells.8
It is known that granulocytes may be part of the inflammatory process in sarcoidosis.9 10 The BAL method used by Facco et al was referenced, via the online supplement, to an original paper that used a 200 ml lavage. A differential cell count seems to have been produced from a cytospin, but in the table listing differential BAL data the percentage of neutrophils was not stated.
It would therefore be of interest if the authors could clarify the methodology used for the BAL and differential cell counts, whether any neutrophils were detected in BAL from people with sarcoidosis, and if so, did neutrophils demonstrate IL-17 immunolocalisation? Such data may support a paradigm indicating that IL-17 expression may involve cells in addition to Th17 lymphocytes in sarcoidosis. This may also be relevant to other lung pathologies where IL-17 is implicated.