C1qb, a gene encoding a subunit of the complement component C1q, is a key player in the complement system, which is involved in immune responses, inflammation, and clearance of pathogens. C1q, composed of C1QA, C1QB, and C1QC, initiates the classical complement pathway upon binding to antibody-antigen complexes [8]. This pathway is crucial for innate and adaptive immunity, influencing various biological processes and disease states.

In primary refractory diffuse large B cell lymphoma, C1QB-expressing macrophages show increased cholesterol efflux, which inhibits CAR-T cell cytotoxicity by inducing an immunosuppressive state in CD8+ T cells, leading to their exhaustion [1]. In colorectal cancer, forward Mendelian randomization analysis indicates that C1QB is a risk factor for CRC, suggesting its oncogenic role [2]. In skin cutaneous melanoma, high levels of C1QB expression are associated with favorable prognosis, and gene set enrichment analysis shows that its expression may be involved in cell-cell interaction, cell behavior, and intracellular signaling transduction [3,8]. In type 1 diabetes mellitus, silencing C1QB inhibits the differentiation of monocytes into macrophages, reduces the number of macrophages, and alleviates pancreatic islet β-cell damage [4]. For diabetic nephropathy, C1QB is identified as a potential candidate gene for diagnosis [5]. In intrahepatic cholangiocarcinoma, an APOE + C1QB+ macrophage subtype is associated with a poor prognosis [6]. In psoriasis complicated with atherosclerosis, C1QB is one of the important hub genes identified [7].

In conclusion, C1qb plays diverse and significant roles in multiple disease conditions, mainly through its involvement in immune-related processes. Research using various models, though not specifically KO/CKO mouse models in the provided references, has revealed its importance in cancers, diabetes-related complications, and inflammatory diseases, enhancing our understanding of disease mechanisms and potentially guiding new therapeutic strategies.