Lyz2, also known as Lysozyme-M, is a gene that plays crucial roles in the immune system. Lysozyme encoded by Lyz2 is involved in innate immunity, particularly in the antibacterial defense mechanism. It hydrolyzes the peptidoglycan layer of bacterial cell walls, thereby contributing to the body's first-line defense against bacterial infections [1].

In various in vivo studies using gene knockout models, Lyz2-Cre-mediated genetic deletion has been utilized to explore its functions. For example, in the study of macrophage cytokinesis and Kras-driven tumorigenesis, crossing septin7-floxed mice with Lyz2-Cre mice (where Cre recombinase is inserted in the Lyz2 gene locus) specifically deleted septin7 in myeloid cells like monocytes, macrophages, and granulocytes. This revealed an essential role of Septin7 in macrophage cytokinesis but not in macrophage function. Also, septin7 was found to be essential for oncogenic Kras-driven lung tumorigenesis [2]. In another case, conditional deletion of Akt1 in macrophages using Akt1(-/-)Lyz2-cre mice showed that Akt1-mediated mitophagy in macrophages contributes to alveolar macrophage apoptosis resistance and is required for pulmonary fibrosis development [3].

In conclusion, Lyz2 is crucial for innate antibacterial immunity. The use of Lyz2-Cre-mediated gene knockout or conditional knockout mouse models has significantly advanced our understanding of Lyz2's role in processes such as macrophage function, cytokine production, and in disease conditions like pulmonary fibrosis and Kras-driven tumorigenesis. These models provide valuable insights into the underlying molecular mechanisms, potentially guiding the development of new therapeutic strategies for related diseases.