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LILRB4, an immune checkpoint on myeloid cells
Ting Yang1, Yixin Qian1, Xiaoting Liang1
1Peking University International Cancer Institute, Health Science Center, Peking University, Beijing, China.
Insights
Leukocyte immunoglobulin-like receptor B4 (LILRB4) is an inhibitory receptor on myeloid cells. It acts as an immune checkpoint, suppressing T cells and offering a potential target for cancer immunotherapy and other immune diseases.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Leukocyte immunoglobulin-like receptor B4 (LILRB4) is an inhibitory receptor within the LILR family.
- It is primarily expressed on human myeloid cells, both normal and malignant.
- LILRB4 plays a role in various physiological and pathological conditions.
Purpose of the Study:
- To elucidate the function of LILRB4 in myeloid cells.
- To explore the role of LILRB4 in disease pathogenesis.
- To evaluate LILRB4 as a potential therapeutic target.
Main Methods:
- Analysis of LILRB4 expression patterns.
- Investigation of LILRB4 signaling pathways upon ligand binding.
- Assessment of LILRB4's impact on T cell function.
- Correlation of LILRB4 expression with disease severity and patient survival.
Main Results:
- LILRB4 activation recruits adaptors to initiate signaling cascades.
- In normal myeloid cells, LILRB4 regulates cell activation and differentiation.
- In malignant myeloid cells, LILRB4 correlates with disease severity and suppresses T cells.
Conclusions:
- LILRB4 functions as an immune checkpoint on myeloid cells.
- LILRB4 is implicated in the pathogenesis of various diseases, including cancer.
- LILRB4 represents a promising therapeutic target for immune diseases and cancer immunotherapy.
Abstract:
Leukocyte immunoglobulin-like receptor B4 (LILRB4) is an inhibitory receptor in the LILR family mainly expressed on normal and malignant human cells of myeloid origin. By binding to ligands, LILRB4 is activated and subsequently recruits adaptors to cytoplasmic immunoreceptor tyrosine inhibitory motifs to initiate different signaling cascades, thus playing an important role in physiological and pathological conditions, including autoimmune diseases, microbial infections, and cancers. In normal myeloid cells, LILRB4 regulates intrinsic cell activation and differentiation. In disease-associated or malignant myeloid cells, LILRB4 is significantly correlated with disease severity or patient survival and suppresses T cells, thereby participating in the pathogenesis of various diseases. In summary, LILRB4 functions as an immune checkpoint on myeloid cells and may be a promising therapeutic target for various human immune diseases, especially for cancer immunotherapy.
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