anti-Leukocyte Immunoglobulin-Like Receptor, Subfamily B (With TM and ITIM Domains), Member 4 (LILRB4) Antibodies

Human Leukocyte Immunoglobulin-Like Receptor, Subfamily B (With TM and ITIM Domains), Member 4 (LILRB4) interaction partners

1. LILRB4 expression is decreased in hypertrophic hearts.

2. Our data demonstrate that anti-LILRB4 CAR-T cells specifically target monocytic acute myeloid leukemia cells with no toxicity to normal hematopoietic progenitors.

3. LILRB4 orchestrates tumour invasion pathways in monocytic leukaemia cells by creating an immunosuppressive microenvironment; LILRB4 represents a compelling target for the treatment of monocytic AML

4. Results suggest that ILT3 played an important role in tumor progression in colorectal cancer by possible influence on CD45RO+ T cells in the tumor microenvironment.

5. These results suggest that tyrosine phosphorylation may be critical in FcgammaRI-dependent endocytosis/phagocytosis that may be regulated by LILRB4 by triggering dephosphorylation of key signalling proteins.

6. ILT3 may functionally contribute to a regulatory network controlling tumor progression by suppressing the Akt pathway.

7. The ILT3 PBs/PCs were suggested to be developmentally equivalent based on the simultaneous generation of these populations upon activation of memory B cells in vitro ILT3 expression was found to be induced efficiently by IL-2, while IFN-alpha effectively induced ILT3 PBs/PCs in vitro Utilizing the elevated ILT3 will support opening a new avenue for molecular markers for, pathogenic cells.

8. this study shows that LILRB4 might have dual inhibitory and activating functions, depending on the position of the functional tyrosine residues in its immunoreceptor tyrosine-based inhibitory motifs and/or the nature of the stimuli

9. LILRB4 expression is significantly upregulated in human masticatory mucosa during wound healing

10. Identification of ILT4 as a cellular receptor for CSP C4d

11. involvement of ILT3 and ILT4 in the modulation of immune responsiveness in multiple sclerosis by both interferon and vitamin D

12. Cyclosporine up-regulated the expression of ILT3 and ILT4 on natural killer cells, which influenced their cytotoxicity against tumor cells.

13. ILT3Fc inhibits T cell activation and induces the generation of suppressor T cells targeting multiple inflammatory miRNA pathways.

14. Crystal structure of leukocyte Ig-like receptor LILRB4 (ILT3/LIR-5/CD85k): a myeloid inhibitory receptor involved in immune tolerance.

15. upregulated on antigen-presenting cells in response to Salmonella infection

16. Data show that LILRB4 is a potent inhibitor of monocyte activation via FcgammaRI.

17. report that ILT2 receptor, ILT3 receptor, ILT4 receptor, and KIR2DL4 receptor expression is up-regulated by HLA-G histocompatibility antigen in antigen-presenting cells, natural killer cells, and T cells

18. ILT3 precursor RNA is expressed and retained in nuclei of resting endothelial cells.

19. Our findings indicate that expression of ILT3 and ILT4 on CLL B cells represents a phenotypic abnormality that may play a role in tolerization of tumor-specific T cells.

20. The inhibitory effect of serum and membrane ILT3 in a humanized SCID mouse model describes an immune-escape mechanism that could contribute to impaired T cell responses in patients with cancer.

Mouse (Murine) Leukocyte Immunoglobulin-Like Receptor, Subfamily B (With TM and ITIM Domains), Member 4 (LILRB4) interaction partners

1. LILRB4 knockout accelerates cardiac hypertrophy induced by aortic banding in mice. LILRB4 deficiency promotes inflammation and apoptosis in aortic banding-stimulated heart injury.

2. Targeting hepatic LILRB4 to improve its expression or activation represents a promising strategy for the treatment of non alcoholic fatty liver diseases as well as related liver and metabolic diseases

3. Results suggest that plasma cell development from memory and marginal zone B cells, as well as subsequent antibody production, are suppressed via glycoprotein 49B (gp49B).

4. LILRB4 can downregulate the development of pathologic allergic inflammation.

5. receptor attenuates the number of these mature DCs and attendant IL-4-producing lymphocytes in the lymph nodes, and accordingly, the ability of DCs to elicit pathologic Th2 pulmonary inflammation

6. Inhibition of anaphylactic inflammation by the gp49B1 receptor on mast cells.

7. Gp49B1 is a unique inhibitory receptor that is induced in multiple lineages of innate and adaptive immune cells during an infection and controls their IFN-gamma, but not cytotoxic responses.

8. Expression of gp49B was detected on peripheral eosinophils of control mice and on eosinophils from lungs of mice treated with RW, suggesting a role for gp49B on eosinophils in dampening allergic inflammatory responses.

9. study reports that gp49B, is expressed on dendritic cells and downregulates cellular activity to prevent the excessive activation of T cells in vitro and in vivo