LILRB1/CD85j/ILT2 Protein, Human (Biotinylated, HEK293, His-Avi)

LILRB1/CD85j/ILT2 Protein is an inhibitory receptor broadly expressed on leukocytes. LILRB1 recognises a wide range of classical HLA-class I allelic variants, as well as the non-classical molecules HLA-F and -G by binding to the conserved a3 domain. LILRB1 also recognises the human CMV-encoded MHC class I homologue UL18. LILRB1 is encoded within the leukocyte receptor complex on 19q13.4. LILRB1 can function as a negative regulator of BiTE molecule-induced tumor cell killing. LILRB1 acts as a novel checkpoint inhibitory molecule capable of restricting BiTE molecule-mediated CD8+ T cell effector function^[1][2][3][4]. LILRB1/CD85j/ILT2 Protein, Human (Biotinylated, HEK293, His-Avi) is the recombinant human-derived LILRB1/CD85j/ILT2 protein, expressed by HEK293 , with C-Avi, C-6*His labeled tag. The total length of LILRB1/CD85j/ILT2 Protein, Human (Biotinylated, HEK293, His-Avi) is 435 a.a., with molecular weight of 70-90 kDa.

LILRB1 binds MHC class I and also contain immunoreceptor tyrosine-based inhibitory motifs involved in the intracellular transduction of inhibitory signaling, which establishes them as strong candidates for MHC class I-mediated suppression of phagocytosis^[1].
LILRB1 and PD1 shows nonoverlapping expression patterns across CD8+ TEM and TEMRA subsets, and blocking both pathways synergistically enhanced CD8+ T cell function. LILRB1 is highly expressed by the CD8+ TEMRA subset, which is the most potent population for BiTE molecule–induced toxicity. LILRB1-expressing CD8+ T cells infiltrate solid tumors. LILRB1 blockade increases CD8+ T cell cytolytic activity in vitro^[3].

Human

HEK293

C-Avi;C-6*His

D9IDM8 (G24-H458)

10859

GHLPKPTLWAEPGSVITQGSPVTLRCQGGQETQEYRLYREKKTAPWITRIPQELVKKGQFPIPSITWEHAGRYRCYYGSDTAGRSESSDPLELVVTGAYIKPTLSAQPSPVVNSGGNVTLQCDSQVAFDGFILCKEGEDEHPQCLNSQPHARGSSRAIFSVGPVSPSRRWWYRCYAYDSNSPYEWSLPSDLLELLVLGVSKKPSLSVQPGPIVAPEETLTLQCGSDAGYNRFVLYKDGERDFLQLAGAQPQAGLSQANFTLGPVSRSYGGQYRCYGAHNLSSEWSAPSDPLDILIAGQFYDRVSLSVQPGPTVASGENVTLLCQSQGWMQTFLLTKEGAADDPWRLRSTYQSQKYQAEFPMGPVTSAHAGTYRCYGSQSSKPYLLTHPSDPLELVVSGPSGGPSSPTTGPTSTSGPEDQPLTPTGSDPQSGLGRH

70-90 kDa

Greater than 95% as determined by reducing SDS-PAGE.

<1 EU/μg, determined by LAL method.