The study shows that the antimicrobial peptide LL‑37 is higher in the skin of people with hidradenitis suppurativa, a painful inflammatory condition, and that it’s linked to immune cells and inflammatory signals. It also finds LL‑37 can make certain T‑cells multiply by raising calcium inside the cells, independent of other immune helpers. This suggests LL‑37 plays a role in driving inflammation, not just fighting microbes.

Hidradenitis suppurativa (HS) is an inflammatory skin disease with poorly understood immunopathogenic mechanisms. LL-37 is an antimicrobial peptide, which is transcribed from the CAMP (cathelicidin antimicrobial peptide) gene. Previous reports showed upregulated levels of CAMP and LL-37 in HS lesions, and therefore, the aim of this study was to compare levels of LL-37 in HS to other inflammatory skin diseases and to establish immunomodulatory functions of LL-37 in HS. We confirm an upregulation of the LL-37 peptide in lesional HS skin with comparable levels as in psoriasis patients and are able to positively correlate the presence of LL-37 in HS with the presence of T cells, macrophages, neutrophils, IFN-γ, IL-17, IL-23, TNF-α, IL-32 and IL-1β. Mechanistically, LL-37 boosts the proliferation of unspecifically activated CD4⁺ T cells via an increased calcium signalling independent of antigen-presenting cells. Targeting LL-37 may therefore represent a new therapeutic option for the treatment of this recalcitrant disease, but it has to be kept in mind that LL-37 also has an antimicrobial function.