• The leukocyte immunoglobulin-like receptor (LILR) family is a group of paired immunoregulatory receptors expressed in human myeloid and lymphoid cell populations, which can be divided into two categories: the inhibitory LILR subfamily B (LILRB1-5) and the activating LILR subfamily A (LILRA1-6). LILRB4, one of the LILR family members, also known as CD85K or ILT3, is primarily expressed on myeloid cells such as monocytes, macrophages, and dendritic cells (DCs). Its cytoplasmic domain contains three immunoreceptor tyrosine-based inhibitory motifs (ITIMs), classifying it as an inhibitory receptor. LILRB4 has a broad range of ligands, including MHC class I molecules, APOE, and CD166, among others. Its primary function is exerted by inhibiting the activity of antigen-presenting cells (APCs), thereby suppressing the activation of CD4+ T cells. Additionally, it serves as a key biomarker for monocytic leukemia, supporting tumor cell infiltration into tissues and inhibiting T cell activity in acute myeloid leukemia (AML) cells. Thus, LILRB4 represents a promising therapeutic target for monocytic acute myeloid leukemia.
• The mouse Lilrb4a and Lilrb4b gene are replaced by the exons 1-12 of human LILRB4 gene that encode signal peptide, extracellular domain, transmembrane domain, and cytoplasmic region in B-hLILRB4 mice(C). The human LILRB4 expression is driven by human LILRB4 promoter, while mouse Lilrb4 gene transcription and translation will be disrupted.
• Human LILRB4 was detectable in dendritic cells, monocytes, macrophages, T cells and B cells of humanized B-hLILRB4 mice(C), but not in NK cells and granulocytes. The human LILRB4 was not expression in wild-type BALB/cCrSICNifdc mice.
• This product is used for the pharmacological evaluation of LILRB4-targeted drugs in oncology.

Gene targeting strategy for B-hLILRB4 mice(C). The mouse Lilrb4a and Lilrb4b gene are replaced by the exons 1-12 of human LILRB4 gene that encode signal peptide, extracellular domain, transmembrane domain, and cytoplasmic region in B-hLILRB4 mice(C). The promoter and 3’ or 5’UTR region also belongs to human. The human LILRB4 expression is driven by human LILRB4 promoter, while mouse Lilrb4 gene transcription and translation will be disrupted.

Strain specific LILRB4 expression analysis in homozygous B-hLILRB4 mice(C) by flow cytometry. Splenocytes were collected from wild-type BALB/cCrSIcNifdc mice (+/+) and humanized B-hLILRB4 mice(C) (H/H) and analyzed by flow cytometry with species-specific anti-human LILRB4 antibody (Biolegend, 333016). Human LILRB4 was detectable in dendritic cells, monocytes, macrophages, T cells and B cells (low) of humanized B-hLILRB4 mice(C), but not in NK cells and granulocytes. The human LILRB4 was not expression in wild-type BALB/cCrSIcNifdc mice.

Strain specific LILRB4 expression analysis in homozygous B-hLILRB4 mice(C) by flow cytometry. Blood cells were collected from wild-type BALB/cCrSIcNifdc mice (+/+) and humanized B-hLILRB4 mice(C) (H/H) and analyzed by flow cytometry with species-specific anti-human LILRB4 antibody (Biolegend, 333016). Human LILRB4 was detectable in dendritic cells, monocytes, macrophages, T cells and B cells (low) of humanized B-hLILRB4 mice(C), but not in NK cells and granulocytes. The human LILRB4 was not expression in wild-type BALB/cCrSIcNifdc mice.

Strain specific analysis of Lilrb4 mRNA expression in wild-type BALB/cCrSIcNifdc and B-hLILRB4 mice(C) by RT-PCR. Spleen RNA were isolated from wild-type BALB/cCrSIcNifdc (+/+) and homozygous B-hLILRB4 mice(C) (H/H), then cDNA libraries were synthesized by reverse transcription, followed by PCR with mouse Lilrb4 primers. Mouse Lilrb4 mRNA was detectable in wild-type BALB/cCrSIcNifdc mice, but not in B-hLILRB4 mice(C).