Research progress of B subfamily of leucocyte immunoglobulin-like receptors in inflammation.
Mengting ZhangJian YangJing ZhangCuiyuan HuangHaiyin LiuPeiyue ZhangYuhong ZhaiLi LiuJian YangPublished in: International journal of immunogenetics (2023)
Leucocyte immunoglobulin-like receptors subfamily B (LILRB) belongs to the type I transmembrane glycoproteins, which is the immunosuppressive receptor. LILRBs are widely expressed in bone marrow cells, hematopoietic stem cells, nerve cells and other body cells. Studies have found that LILRBs receptor can bind to a variety of ligands and has a variety of biological functions such as regulating inflammatory response, immune tolerance and cell differentiation. Inflammatory reaction plays a vital role in resisting microorganisms. The function of inhibitory immune receptors can recognize the signs of infection and promote the function of anti-microbial effect. The inflammatory response must be strictly regulated to prevent excessive inflammation and tissue damage. Therefore, it is of general interest to understand the role of LILRBs in the inflammatory response. Because they can inhibit the anti-microbial response of neutrophils, some human pathogens use these receptors to escape immunity. This article reviews the biological role of LILRBs in the inflammatory response. We focus on the known ligands of LILRBs, their different roles after binding with ligands, and how these receptors help to form neutrophil responses during infection. Recent studies have shown that LILRBs recruit phosphatases through intracellular tyrosine-based immunoreceptor inhibitory motifs to negatively regulate immune activation, thereby transmitting inflammation-related signals, suggesting that LILRBs may be an ideal target for the treatment of inflammatory diseases. Here, we describe in detail the regulation of LILRBs on the inflammatory response, its signal transduction mode in inflammation, and the progress in the treatment of inflammatory diseases, providing a reference for further research.
Keyphrases
- inflammatory response
- oxidative stress
- induced apoptosis
- lipopolysaccharide induced
- lps induced
- bone marrow
- toll like receptor
- stem cells
- cell cycle arrest
- mesenchymal stem cells
- endoplasmic reticulum stress
- immune response
- systematic review
- cell death
- microbial community
- randomized controlled trial
- transcription factor
- combination therapy
- binding protein
- cell therapy
- physical activity
- reactive oxygen species
- antimicrobial resistance