Abstract
Background: IL-17A has been linked to different chronic lung diseases associated with respiratory failure leading to lung transplantation. IL-17A secretion has been mainly attributed to conventional CD3+CD4+ Th17 cells. The contribution of innate lymphocytes (innate lymphoid cells; ILCs, gamma-delta T cells and inducible natural killer T cells; iNKT) to IL-17A in end stage lung diseases remains largely unexplored.
Methods: We analyzed 14-20 lymph node (LN) and lung tissue samples derived from lung explants prior to lung transplantation from cystic fibrosis, emphysema and fibrosis patients as well as LN samples from lung donors as controls. IL-17A secretion was detected by flow cytometry of single cells suspensions. Supernatants and RNA from single cell suspensions were assessed via multiplex technology to characterize cytokine and molecular pathway patterns associated with IL-17A secreting lymphocytes.
Results: A significant proportion of IL-17A secretion (22-44%) remained unaccounted for by flow cytometric analysis of conventional T helper cells. We detected secretion of IL-17A by innate lymphoid, gamma delta T cells and iNKT cells. Analysis of supernatants and RNA via multiplex technology revealed that IL-17A secretion was accompanied by several IL-17A-associated cytokines and molecular pathways suggested to play a role in end stage lung disease.
Conclusion: We identified production of IL-17A among populations of ILCs, gamma delta T cells and iNKT cells in different lung disease entities which suggests that these cell populations can contribute to IL-17A-dependent pathologies in end stage lung disease.
Footnotes
Cite this article as: European Respiratory Journal 2018 52: Suppl. 62, PA1119.
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- Copyright ©the authors 2018