This record provides bibliographic details and links to the original research. An editorial study breakdown is not available.
What the researchers found
Substance P amplified the pathogenicity of GM-CSF-producing T helper cells in dry eye disease through the NK1R receptor. Blocking NK1R reduced disease severity in a mouse model.
Why it matters
Dry eye disease is an inflammatory condition where neuropeptides and immune cells interact. Identifying the substance P-NK1R axis as a driver opens a new therapeutic target for this common condition.
The numbers in context
Substance P increased GM-CSF expression in ThGM cells. NK1R-expressing ThGM transfer significantly exacerbated DED. NK1R-knockdown ThGM weakly aggravated DED. NK2R knockdown had no effect.
How the study worked
Murine dry eye disease model. Characterized NK1R and NK2R expression on ThGM and Th1 cells. Substance P and NKA stimulation assays. Adoptive transfer of NK1R-expressing vs. NK1R-knockdown ThGM cells.
Who was studied
Mice with induced dry eye disease
What this study cannot tell us
Mouse model only. DED in humans may involve different immune mechanisms. Adoptive transfer experiments are artificial. NK1R antagonists not tested therapeutically.
Read the original research
Substance P and neurokinin 1 receptor boost the pathogenicity of granulocyte-macrophage colony-stimulating factor-producing T helper cells in dry eye disease.
Scandinavian journal of immunology, 101(1), e13434
Citation
Rong, Hua; Yang, Hai; Liu, Qingqing; Zhang, Hui; Wang, Shaolin. (2025). Substance P and neurokinin 1 receptor boost the pathogenicity of granulocyte-macrophage colony-stimulating factor-producing T helper cells in dry eye disease.. Scandinavian journal of immunology, 101(1), e13434. https://doi.org/10.1111/sji.13434