Mouse Leukocyte Immunoglobulin-like Receptor Subfamily B Member 4 (LILRB4/CD85k/ILT3) is an approximately transmembrane glycoprotein that negatively regulates immune cell activation. Mouse LILRB4 consists of a 215 amino acid (aa) extracellular domain with two Ig-like domains, a 22 aa transmembrane segment, and a 75 aa cytoplasmic domain with 3 immunoreceptor tyrosine-based inhibitory motifs (ITIM). Within the ECD, mouse LILRB4 shares 45% and 77% aa sequence identity with human and rat LILRB4, respectively. Alternative splicing of mouse LILRB4 generates a potentially soluble isoform that lacks the transmembrane segment. LILRB4 is expressed on dendritic cells (DC), monocytes, macrophages, and vascular endothelial cells (EC). Ligation of LILRB4 triggers ITIM-mediated inhibition of cellactivating signaling, leading to enhanced immune tolerance and reduced allogeneic graft rejection. Soluble LILRB4 induces the differentiation of CD8+ T suppressor cells (Ts) that can inhibit the effector functions of CD4+ Th cells and CD8+ CTL. In turn, CD8+ Ts cells induce LILRB4 up-regulation and a tolerogenic phenotype in monocytes, DC, and EC.
Mouse Leukemia inhibitory factor（lif）is a secreted protein which belongs to the LIF/OSM family.LIF has been implicated in a many physiological processes including development, hematopoiesis, bone metabolism, and inflammation. it has the capacity to induce terminal differentiation in leukemic cells. Its activities include the induction of hematopoietic differentiation in normal and myeloid leukemia cells, the induction of neuronal cell differentiation, and the stimulation of acute-phase protein synthesis in hepatocytes.
LIFR (leukemia inhibitory factor receptor) belongs to the family of cytokine receptors. LIFR forms a high-affinity receptor complex with gp130, which mediates the activity of LIF (leukemia inhibitory factor) and thus affects the differentiation, proliferation, and survival of a wide variety of cells in the adult and the embryo. Besides LIF, LIFR can also bind to and activate CNTF (ciliary neurotrophic factor) and CLC (cardiotrophin like cytokine). Evidence showed that in the retina, LIFR activating LIF, CT-1 and cardiotrophin like cytokine (CLC) are strongly upregulated in response to preconditioning with bright cyclic light leading to robust activation of signal transducer and activator of transcription-3 (STAT3) in a time-dependent manner. Further, blocking LIFR activation during preconditioning using a LIFR antagonist (LIF05) attenuated the induced STAT3 activation and also resulted in reduced preconditioning-induced protection of the retinal photoreceptors. These data demonstrate that LIFR and its ligands play an essential role in endogenous neuroprotective mechanisms triggered by preconditioning-induced stress. LIFR was newly found to be a suppressor of hepatocellular carcinoma (HCC), one of the world's top five causes of cancer-related deaths.
Cytokine that binds to TNFRSF3/LTBR. Binding to the decoy receptor TNFRSF6B modulates its effects. Activates NFKB and stimulates the proliferation of T-cells. Acts as a ligand for TNFRSF14/HVEM. Upon binding to TNFRSF14/HVEM, delivers costimulatory signals to T cells, leading to T cell proliferation and IFNG production.
LIGHT , also known as TNFSF14 or CD258 , is a newly identified member of the TNF superfamily (TNFSF14) that is expressed by activated T lymphocytes , monocytes , granulocytes , spleen cells , and immature dendritic cells. TNFSF14 / LIGHT / CD258 is a type II transmembrane protein that is known to bind 2 membrane-bound TNFSF signaling receptors: HVEM , which is predominantly expressed by T cells , and lymphotoxin β receptor (LTβR) , which is expressed by stromal cells and nonlymphoid hematopoietic cells. TNFSF14 / LIGHT / CD258 also binds to a soluble non-signaling receptor , decoy receptor 3 (DcR3) , which can modulate the function of LIGHT in vivo. TNFSF14 / LIGHT / CD258 can also costimulate T cell responses via HVEM , which is constitutively expressed in most lymphocyte subpopulations , including CD4+ and CD8+ T cells. In addition , TNFSF14 / LIGHT / CD258 has been shown to suppress tumor formation in vivo and to induce tumor cell apoptosis via the up-regulation of intercellular adhesion molecule 1 and an increased lymphocyte adhesion to cancer cells. Thus , TNFSF14 / LIGHT / CD258 is being actively investigated as a possible basis for cancer treatment.
Leukocyte immunoglobulin-like receptor subfamily B member 3, also known as Leukocyte immunoglobulin-like receptor 3, Immunoglobulin-like transcript 5, Monocyte inhibitory receptor HL9, CD85 antigen-like family member A, CD85a and LILRB3, is a single-pass type I membrane protein which belongs to the leukocyte receptor cluster (LRC) present on 19q13.4. LILRB3 / CD85a contains fourIg-like C2-type (immunoglobulin-like) domains. LILRB3 / CD85a contains three copies of a cytoplasmic motif that is referred to as the immunoreceptor tyrosine-based inhibitor motif (ITIM). This motif is involved in modulation of cellular responses. The phosphorylated ITIM motif can bind the SH2 domain of several SH2-containing phosphatases. LILRB3 / CD85a is expressed on immune cells where it binds to MHC class I molecules on antigen-presenting cells and transduces a negative signal that inhibits stimulation of an immune response. It is thought to control inflammatory responses and cytotoxicity to help focus the immune response and limit autoreactivity. Multiple transcript variants encoding different isoforms have been found.
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