Itgb2, also known as integrin beta 2, is a gene that plays a crucial role in coordinating extracellular and intracellular signaling. Integrins are known to reshape the tumor microenvironment, and Itgb2 is involved in host defense [1]. It has been associated with pathways such as PI3K/AKT/mTOR, which regulate cellular metabolism and growth [1].

In oral squamous cell carcinoma (OSCC), CAFs with higher Itgb2 expression promoted tumor cell proliferation. Itgb2 regulated the PI3K/AKT/mTOR axis to enhance glycolysis in CAFs, and the lactate produced was absorbed by OSCC cells, which then oxidized NADH in the mitochondrial oxidative phosphorylation system to generate ATP [1]. In non-small cell lung cancer, lncRNA ITGB2-AS1 was found to promote cisplatin resistance by inhibiting ferroptosis via activating the FOSL2/NAMPT axis [2]. In severe acute pancreatitis-related acute lung injury, extracellular vesicles overexpressing ITGAM and ITGB2 could attenuate pulmonary inflammation and endothelial cell barrier disruption [3]. In cerebral ischemia-reperfusion injury, Itgb2+ microglia subclusters were involved in energy metabolism, cell cycle, angiogenesis, neuronal myelin formation, and repair at different time points [4]. In glioblastoma, ITGB2 in microglia promoted the mesenchymal transition of GBM cells through the JAK1/STAT3/IL-6 signaling feedback [5]. In diabetic nephropathy, ITGB2 was identified as a potential diagnostic marker [6]. In inflammatory bowel disease, suppression of ITGB2 expression alleviated inflammation in mice, and it may be a potential diagnostic marker for IBD-associated colorectal cancer [7]. In BAP1-mutated uveal melanoma, the ITGB2-ICAM1 axis promoted liver metastasis by preserving hypoxia-and ECM-related signatures [8]. In gliomas, ITGB2 was elevated in higher-malignancy tumors, predicted poor prognosis, and high ITGB2 expression was associated with a better immunotherapy response [9]. In premature infants with necrotizing enterocolitis, although ITGB2 variants were not associated with NEC in the entire cohort, there was a trend towards enrichment with NEC severity in extremely low birthweight infants [10].

In conclusion, Itgb2 is essential in various biological processes and diseases. Studies using different experimental models, though not always gene-knockout or conditional-knockout mouse models, have revealed its role in tumor progression, drug resistance, inflammation-related injuries, and neurodegenerative and kidney diseases. These findings contribute to understanding the molecular mechanisms underlying these diseases and may provide potential therapeutic targets.