Integrins are cell-surface receptors expressed on all cells, except red blood cells. These proteins play important roles in cell proliferation and migration, apoptosis, tissue repair, as well as in all processes critical to inflammation, infection, and angiogenesis. Integrin subunit beta 2 (ITGB2) is coded by the Itgb2 gene. &beta;2 integrins are expressed on all leukocytes and are essential for leukocyte recruitment, as well as other immunological processes. &beta;2 integrin activation regulates cell:cell adhesion when responding to inflammatory signals. To further investigate &beta;2 integrin activation conformations, kinetics, and locations in vivo, the donating laboratory created this humanized &beta;2 knock-in mouse model (hITGB2 KI). Using two activation-specific monoclonal antibodies, mAb KIM127 and mAb24, along with intravital imaging technology, the donating investigator was able to assess local spatiotemporal dynamics after CXCL1- or LPS-induced inflammation. These mice may be a valuable tool for studying immunodeficiency disease such as Leukocyte Adhesion Deficiency Type I (LAD I), as well as evaluating &beta;2-integrin function, activation, kinetics, and bio-distribution in vivo. The floxed hITGB2 homozygous knock-in mice are viable and fertile with no overt phenotype. To date (June 2022), this floxed allele has not been crossed to a cre-recombinase line to produce the knock-out.

Human ITGB2 knock-in/knock-out mice (hITGB2 KI) have a floxed human ITGB2 isoform 1 cDNA sequence replacing exon 2 of the mouse Itgb2 gene. Before exposure to Cre recombinase, this expresses hITGB2 instead of endogenous Itgb2. Upon exposure to Cre recombinase, this is designed to be a knock-out allele. These mice may be a valuable tool for studying immunodeficiency disease such as Leukocyte Adhesion Deficiency (LAD), as well as evaluating &beta;2-integrin function, activation, kinetics, and bio-distribution in vivo.