Table 1.

Distribution of β2 integrins and phenotypes of engineered gene knockout mice.

	Distribution	Phenotypes of knockout mice
αLβ2	All leukocytes but predominates on lymphocytes	Defective adhesion and migration of neutrophils, monocytes, and macrophages; impaired neutrophil chemotaxis; a defect in TNF-α-induced neutrophil and monocyte extravasation from blood vessels; a defect in the induction of peripheral immune responses; reduced NK cytotoxicity.	(14–16)
αMβ2	Abundant on myeloid cells, monocytes/macrophages, neutrophils, NK cells, fibrocytes, mast cells, B cells, CD8+ T cells, and CD4+ γδ T cells	Defective recruitment of neutrophils and mast cells to bacterial and fungal pathogens; a defect in neutrophil binding to fibrinogen and degranulation; impaired mast cell development and innate immunity; a defect in macrophage egression from the peritoneal cavity.	(14, 15)
αXβ2	Abundant on myeloid dendritic cells, monocytes/macrophages; expressed on human NK cells and lymphocyte subpopulations	Defect in intraperitoneal recruitment and adhesive functions of monocytes and macrophages and their ability to kill/phagocytose pathogens.	(17, 18)
αDβ2	Abundant on myeloid cells, macrophages, neutrophils, and monocytes; highly expressed on human NK cells, B cells, and γδT cells	Defective macrophage retention and reduced neutrophil accumulation in the atherosclerotic lesions; defective accumulation of mononuclear cells and neutrophils in the peritoneal cavities of mice infected by S. typhimurium; reduced lung macrophages and increased blood neutrophils in mice with cecal ligation and puncture sepsis or LPS-induced endotoxemia.	(19–22)