CD89, also known as Fcα receptor (FCAR), is a receptor on the surface of various immune cells and belongs to the Fc receptor family. Fc receptors bind antibodies, linking the immune system’s recognition of pathogens with cellular immune responses. CD89 is primarily expressed on monocytes/macrophages, neutrophils, eosinophils, dendritic cells, and Kupffer cells in the liver, unlike other Fc receptors expressed on lymphocytes ^[1]. The function of CD89 primarily involves binding with IgA antibodies (especially IgA1 and IgA2), initiating various immune responses. CD89 can trigger phagocytosis (engulfing and destroying pathogens), antibody-dependent cellular cytotoxicity (ADCC) (killing infected or cancerous cells), and release inflammatory mediators (promoting inflammatory responses and recruiting immune cells) ^[2]. IgA nephropathy (IgAN) is a disease closely associated with CD89 and is the most common form of glomerulonephritis, characterized by the deposition of IgA (particularly IgA1) in the glomeruli. As the myeloid cell-specific Fc receptor for IgA, CD89 specifically binds IgA1, a highly glycosylated IgA subtype predominantly found in serum and responsible for neutralizing pathogens at mucosal surfaces ^[3-4]. In IgA nephropathy, one pathological mechanism is the formation of immune complexes between aberrantly glycosylated IgA1 and CD89. These complexes deposit in the glomerular mesangium, activate mesangial cells and trigger inflammation, fibrosis, and kidney structural damage. Without treatment, the condition can progress to chronic kidney disease (CKD) and even end-stage renal disease (ESRD) ^[5-7].

Since mice lack a homologous gene to human CD89, introducing the human CD89 gene into mice aids in studying immune mechanisms and IgA nephropathy (IgAN). The Cd11b-hCD89 (FCAR) mouse is a humanized model constructed by integrating the coding sequence (CDS) of the human CD89 gene downstream of the stop codon in the mouse Cd11b (Itgam) gene. The human CD89 gene, regulated by the mouse Cd11b gene promoter, is specifically expressed in myeloid cells. Cd11b-hCD89 (FCAR) mice successfully express the human FCAR gene, with the human FCAR protein detectable in peritoneal myeloid cells. Therefore, Cd11b-hCD89 (FCAR) mice can be used to study immune responses, autoimmune mechanisms, tumors, and infectious diseases. They can also be crossed with IgA1 humanized mouse models (catalog number: C001565) to create IgA nephropathy (IgAN) mouse models that better reflect human genetic mechanisms and pathological phenotypes ^[8], facilitating research into IgAN mechanisms and the development of therapies.