Adaptive and innate lymphocyte populations contribute to interleukin (IL)-17A-dependent pathologies in the end-stage of chronic lung diseases such as idiopathic pulmonary fibrosis (IPF) and cystic fibrosis (CF), according to a new study published in Clinical and Translational Immunology. The study also showed that pathogens drive the secretion of IL-17A.

IL-17A and IL-22 play an important role in airway defense, lung repair, and lung homeostasis. IL-17A is crucial for the protection against pulmonary pathogens while IL22 promotes host defense and repair mechanisms in the airways. However, the role of adaptive vs innate lymphocytes in the secretion of IL-17A and IL-22 during end-stage lung disease is not known.

To clarify the patterns specific to different tissues and during different diseases, a team of researchers led by Anna-Maria Dittrich, MD, from the Pediatric Pneumology, Allergology, and Neonatology Unit at Hannover Medical School in Germany compared the secretion patterns of IL-17A and IL-22 in IPF, CF, and emphysema.


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The results showed that IL-17A and IL-22 were secreted by CD4+, CD8+, γδ, and invariant natural killer T cells and innate lymphoid cells in the end-stage of all 3 diseases.

“Our analyses revealed disease-specific contributions of individual lymphocyte subpopulations to cytokine secretion patterns,” the researchers wrote.

They also reported that they found the high levels of microbial detection in samples obtained from patients with CF were associated with a “more pronounced IL-17A signature” compared to other diseases as well as lung donors.

The researchers concluded that lung infections trigger different lymphocyte subpopulations to secrete IL-17A and IL-22. This “converges in end-stage lung diseases and thus provide an IL-17A-enriched milieu promoting progression of tissue destruction and fibrosis,” they said. They added that the development of end-stage lung disease might occur faster in CF due to increased microbial load.

Reference

Albrecht M, Halle O, Gaedcke S, et al. Interleukin-17A and interleukin-22 production by conventional and non-conventional lymphocytes in three different end-stage lung diseases. Clin Transl Immunol. Published online June 16, 2022. doi:10.1002/cti2.1398