LL-37

Ten publications are cited, from 2020 to 2026. Three are human observational studies that measured the body's own LL-37: in breast implant capsule tissue, in the saliva of children and adolescents living with HIV in Kenya, and in the saliva and serum of people with rheumatoid arthritis and chronic periodontitis. Seven are preclinical. Three used mice, in models of high cholesterol, diabetic wounds and MRSA-infected wounds, and four are laboratory studies of human keratinocytes, human osteoblast-like cells, coronary artery endothelial cells in Kawasaki disease, and Rift Valley fever virus.

In implant capsules, LL-37 was found in macrophages and myofibroblasts, and the more severe the capsular contracture, the less of it was expressed. The periodontitis study reported that rheumatological and periodontal measures correlated, while the HIV study called for longitudinal research. In diabetic mice, LL-37 was reported to accelerate wound closure through TFEB-dependent autophagy, and the MRSA study's authors pointed to infected wounds as an area for future work. A 2026 study found that LL-37 interacts with apolipoprotein B-100 to promote LDL clearance, and that the mouse homologue, CRAMP, sped cholesterol clearance in hypercholesterolaemic Apoe-/- mice. In cells, LL-37 induced CXCL10 in keratinocytes through Jak1/STAT1, which the authors linked to T-cell-driven rosacea; triggered inflammatory signalling through TLR4, NF-κB and NLRP3 in Kawasaki disease endothelial cells; reduced the viability of osteoblast-like cells at the concentration tested; and showed time-dependent activity against Rift Valley fever virus.

None of the cited work gives LL-37 to people: the human studies measure the peptide already present, and two of them report correlations. The animal evidence comes from mice, and one study relied on the mouse homologue rather than LL-37 itself. Each finding rests on a single study, and the findings point in different directions, with the peptide appearing as a driver of inflammation in the rosacea and Kawasaki models, as a participant in repair in diabetic mice, and as toxic to osteoblast-like cells in culture.