Recombinant type XVII humanized collagen improves skin damage of mice with systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is a complex immunological disorder disease, with skin lesions being one of its most common clinical manifestations. Collagen type XVII is primarily localized in the basement membrane of the skin, anchoring the epidermis to the dermis. Disruption of collagen type XVII leads to autoimmune blistering skin conditions. In this study, we observed that recombinant type XVII humanized collagen (rhCOL17) bound to the cell membrane of human fibroblasts (HFBs) without entering into the cells. RhCOL17 regulated cellular behaviors, including cell morphology, proliferation and adhesion. Additionally, rhCOL17 mitigated the inflammatory response and the expression of SLE-related genes in HFB cells. Therefore, we hypothesized that rhCOL17 has the potential to alleviate SLE-induced skin damage. To test this hypothesis, rhCOL17 was injected into the site of skin damage of MRL/lpr mice, a well-established animal model of SLE characterized by significant skin damage. The results demonstrated that subcutaneous injection of rhCOL17 resulted in a reduction of SLE serum markers in MRL/lpr mice, along with improvements of skin damage and lesions in kidneys and spleens. Furthermore, rhCOL17 reduced the inflammatory response of MRL/lpr mice skin. These findings suggest that rhCOL17 is prospective as a therapeutic option for SLE-induced skin injury.