H2-Ab1, also known as histocompatibility 2, class II antigen A, beta 1, is a gene encoding the beta chain of the Class II heterodimer H2-A, which is a major histocompatibility complex (MHC) class II protein. MHC class II proteins are involved in the immune response by presenting antigens to CD4+ T cells, thus playing a crucial role in activating the adaptive immune system [4].

In a study on pulmonary arterial hypertension (PAH), H2-Ab1 was identified as a key gene. Knocking down H2-Ab1 in mouse pulmonary artery endothelial cells (PAECs) inhibited cell viability, adhesion, migration, and angiogenesis, while promoting apoptosis, indicating its role in PAH vascular remodeling [1].

In allergic rhinitis, double knockout of H2-Ab1 and H2-Eb1 in mice reduced the susceptibility to the disease, with fewer histological changes in nasal mucosa, reduced eosinophilic granulocytes and mast cells, and altered Th1/Th2 cell factor balance [2].

In colitis mouse models, disruption of H2-Ab1 in intestinal epithelial cells (IECs) led to less severe DSS-or T-cell transfer-induced colitis, but also reduced bacterial clearance in Citrobacter rodentium-induced colitis due to decreased IgA binding to bacteria [3].

In renal fibrosis models, global or renal tubule-specific ablation of H2-Ab1 alleviated fibrosis, with changes in renal CD4+ T cell subsets and profibrotic gene expression [5].

In conclusion, H2-Ab1 is essential for the normal function of the immune response through its role in antigen presentation. Gene knockout studies in mice have revealed its significance in multiple disease conditions such as PAH, allergic rhinitis, colitis, and renal fibrosis. These findings contribute to understanding the pathogenesis of these diseases and may provide potential therapeutic targets related to H2-Ab1-mediated immune regulation.