The CCL1 (C-C motif chemokine ligand 1) gene, located on the q-arm of chromosome 17, encodes a small glycoprotein (approximately 15-16 kDa) belonging to the CC chemokine family. This protein, also known as I-309, is primarily expressed by activated T cells, monocytes/macrophages, and endothelial cells ^[1]. Its main function is as a chemoattractant, specifically drawing monocytes/macrophages, T lymphocytes (especially Th2-differentiated T cells and regulatory T cells), and some dendritic cells to sites of inflammation and immune responses. CCL1 exerts its effects by binding to the chemokine (C-C motif) receptor 8 (CCR8), which is found on various immune cells ^[2]. Beyond its role in immune cell trafficking, CCL1 has antimicrobial activity against bacteria like E. coli and S. aureus, and it can inhibit apoptosis in certain cell lines via the RAS/MAPK pathway ^[3]. CCL1 is implicated in various inflammatory and immune-related disorders, including asthma, atopic dermatitis, rheumatoid arthritis, chronic obstructive pulmonary disease (COPD), tuberculosis, and certain cancers like breast cancer, cervical cancer, and Kaposi Sarcoma, where its dysregulation can contribute to disease pathogenesis ^[3-4]. Cellular tissues where CCL1 expression is notable include the thymus, muscle, stomach, and various immune cells such as T cells, monocytes, B cells, and endothelial cells ^[4]. The B6-hCCL1 mouse is a humanized model, constructed by replacing the coding sequences of the endogenous mouse Ccl1 gene with the coding sequences of the human CCL1 gene. B6-hCCL1 mice can be used for research into the pathogenesis of various inflammatory and immune-related disorders, including asthma, atopic dermatitis, rheumatoid arthritis (RA), chronic obstructive pulmonary disease (COPD), tuberculosis, and certain cancers like breast cancer, cervical cancer, and Kaposi Sarcoma, as well as for the development of CCL1-targeted drugs.

C-C motif chemokine ligand 1 (CCL1), also known as I-309, is a small chemokine mainly secreted by activated T cells, monocytes, and endothelial cells. It belongs to the CC chemokine family and plays a key regulatory role in Th2-type immune responses and the recruitment of regulatory T cells (Tregs) ^[1]. CCL1 binds to its specific receptor CCR8 (C-C chemokine receptor type 8) to mediate the directed migration of Th2 cells and Tregs to inflammatory sites and the tumor microenvironment, promoting the formation of an immunosuppressive tumor microenvironment (TME). It is also involved in the immune regulation of allergic inflammatory responses, autoimmune diseases, and graft-versus-host disease (GvHD) ^[2-3]. The CCL1 gene is located on human chromosome 17 (17q12) and is closely associated with immune evasion in various solid tumors, Th2-type allergic diseases, and the development of inflammatory bowel disease (IBD). Targeting the CCL1-CCR8 signaling axis has become an important strategy for drug development in tumor immunotherapy, allergic diseases, and autoimmune disorders ^[4-5]. The huCCL1(BALB/c) mouse is a humanized model constructed through gene editing technology. The sequences from the start codon to the stop codon of the endogenous mouse Ccl1 gene were replaced with the sequences from the start codon to the stop codon of the human CCL1 gene. This model is suitable for evaluating the efficacy and safety of CCL1-targeted antibodies and CAR-T/CAR-NK cell therapies, as well as for preclinical research in tumor immunity, Th2/Treg immune regulation, allergic disorders, and autoimmune diseases.

Eddm3b is located on chromosome 14 of mice. SgRNA and ssDNA will be designed using Nuclease Technology; Eddm3b conditional knockout mice will be obtained by high-throughput electroporation of fertilized eggs. After sexual maturity, sperm will be collected for cryopreservation.

Skint10 is located on chromosome 4 of mice. Nuclease Technology will be used to design sgRNA; Skint10 knockout mice will be obtained by applying high-throughput electroporation of fertilized eggs. After sexual maturity, sperm were collected for cryopreservation.