Mmp19, a member of the matrix metalloproteinases (MMPs) family, is a zinc-dependent endopeptidase. MMPs play crucial roles in remodeling the extracellular matrix and are involved in various physiological and pathological processes [1,4,5,7]. Mmp19 has been associated with pathways related to cell-matrix interactions, cell migration, and tissue repair [1,3,6].

In animal models, MMP19-deficient mice showed impaired T cell-mediated immune reactions in contact hypersensitivity, with limited inflammatory cell influx, low keratinocyte proliferation, and reduced activated CD8(+) T cells. The development of thymocytes was also altered, suggesting Mmp19 is essential for T cell development and cutaneous immune responses [6]. In pulmonary fibrosis, MMP19 promoted endothelial-to-mesenchymal transition (E(nd)MT), monocyte infiltration, and endothelial barrier permeability. Blocking its interacting proteins SDF1 and ET1 alleviated fibrosis, indicating a potential therapeutic target [1]. In idiopathic pulmonary fibrosis (IPF), MMP19 variants were identified in familial and sporadic cases, with plasma levels higher in patients, providing new clues to IPF pathogenesis [2].

In conclusion, Mmp19 is important for T cell development and cutaneous immune responses. In disease areas, it has a significant impact on pulmonary fibrosis and IPF. Studies using gene-knockout mouse models have revealed its roles in these biological processes and diseases, contributing to a better understanding of related mechanisms and potential therapeutic strategies.