An international research team led by Dr. Wolfgang Merkt from Heidelberg University Hospital has identified a new immunological mechanism that plays a role in fibrotic lung diseases in the context of rheumatic diseases. In the long term, the results could lead to a novel therapeutic principle.

The study focuses on so-called senescent fibroblasts – permanently damaged cells that accumulate in fibrotic lung tissue and promote chronic inflammation and scarring. These cells activate a kind of “immune brake” via the molecule HLA-E that blocks natural killer cells (NK cells). As a result, they evade the natural immune defense.

In preclinical models, the blockade could be lifted by the therapeutic antibody monalizumab. The NK cells became active again and specifically destroyed the senescent fibrosis cells.

The German Society for Rheumatology and Clinical Immunology (DGRh) evaluates the results as an important innovative impulse for rheumatological research. Prof. Dr. med. Ulf Wagner, President of the DGRh, explained that the study may enable a novel therapeutic principle for fibrotic lung diseases in rheumatic patients.

The work combines modern single-cell and tissue analyses with investigations on human samples. It is particularly relevant that the antibody used monalizumab is already being clinically tested in cancer medicine. This could shorten the path to clinical trials in fibrotic lung diseases.

The study was published in the journal Science Translational Medicine . The results suggest that immunological strategies could not only stop fibrotic processes, but possibly partially reverse them. However, further research is needed to translate the findings into clinical application.

Original Paper:

Wolfgang Merkt et al. Natural killer cell immunotherapy reverses lung fibrosis by eliminating senescent fibroblasts. Sci. Transl. Med.18,eadq5442(2026). DOI:10.1126/scitranslmed.adq5442

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Editor: X-Press Journalistenbüro GbR

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