Itgb2, also known as integrin beta 2, is a key coordinator of extracellular and intracellular signaling. Integrins play a significant role in various biological processes such as cell adhesion, migration, and signal transduction. Itgb2 is involved in pathways like PI3K/AKT/mTOR, which regulate cellular metabolism and growth [1].

In oral squamous cell carcinoma (OSCC), CAFs with high Itgb2 expression promote tumor proliferation. Itgb2 regulates PI3K/AKT/mTOR to enhance glycolysis in CAFs, and the lactate produced is absorbed by OSCC cells, generating NADH which is oxidized in the mitochondrial oxidative phosphorylation system to produce ATP [1].

In non-small cell lung cancer, lncRNA Itgb2-AS1 promotes cisplatin resistance by inhibiting ferroptosis via activating the FOSL2/NAMPT axis [2].

In severe acute pancreatitis-related acute lung injury, extracellular vesicles expressing Itgb2 can mediate the process, and overexpressing Itgb2 on engineered EVs can attenuate pulmonary inflammation [3].

In cerebral ischemia-reperfusion injury, Itgb2+ microglia subclusters are involved in energy metabolism, cell cycle, angiogenesis, neuronal myelin formation, and repair at different time points after injury [4].

In glioblastoma, the activation of Itgb2 in microglia promotes the mesenchymal transition of GBM cells through JAK1/STAT3/IL-6 signaling feedback [5].

In diabetic nephropathy, Itgb2 was identified as a potential hub gene, being up-regulated and showing excellent diagnostic efficacy [6].

In inflammatory bowel disease, Itgb2 is up-regulated, and its suppression alleviates inflammation; it may also be a potential diagnostic marker for IBD-associated CRC [7].

In BAP1-mutated uveal melanoma, the Itgb2-ICAM1 axis promotes liver metastasis by preserving hypoxia-and ECM-related signatures [8].

In gliomas, high Itgb2 expression is associated with higher malignancy, poor prognosis, and a better response to immunotherapy [9].

In premature infants with necrotizing enterocolitis, although ITGB2 variants were not associated with NEC in the entire preterm cohort, there was a trend towards enrichment with NEC severity in extremely low birthweight infants [10].

In conclusion, Itgb2 is crucial in multiple biological processes and disease conditions. Studies, including those using gene-based models (although not specifically KO/CKO mouse models in all cases here), have revealed its role in tumor proliferation, drug resistance, inflammation-related injuries, neurodegenerative-like conditions, and potential diagnostic applications in various diseases.