This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
Facts about T-lymphocyte surface antigen Ly-9.
May participate in adhesion reactions between T lymphocytes and accessory cells by homophilic interaction. Promotes T-cell differentiation into a helper T-cell Th17 phenotype leading to greater IL-17 secretion; the costimulatory activity demands SH2D1A (PubMed:22184727).
Human | |
---|---|
Gene Name: | LY9 |
Uniprot: | Q9HBG7 |
Entrez: | 4063 |
Belongs to: |
---|
No superfamily |
CD229 antigen; CD229; cell-surface molecule Ly-9; hly9; Ly9; lymphocyte antigen 9Cell surface molecule Ly-9; mLY9; SLAMF3; T-lymphocyte surface antigen Ly-9
Mass (kDA):
72.139 kDA
Human | |
---|---|
Location: | 1q23.3 |
Sequence: | 1; NC_000001.11 (160796112..160828256) |
Increased surface expression on T-cells of systemic lupus erythematosus (SLE) patients.
Membrane; Single-pass type I membrane protein. Cell membrane.
LY9 is a negative regulator of the development and homeostasis of thymic innate-like CD8+, iNKT cells, and B cells. Boster Bio offers high-affinity primary antibodies to this antigen. This marker can help in many scientific studies, and scientists from around the world can benefit from it. This article will highlight some of the most common uses for LY9.
High-affinity primary antibodies can be used for a variety of applications, including immunohistochemistry (IHC) and Western blotting. These antibodies are tested in IHC, WB, and IP. Boster Bio also provides high-affinity antibodies against other markers, such as LY6. These antibodies are available in 100-ull Liquid format.
The unique role of the LY9 cell surface receptor in modulating innate T cell function is unprecedented. LY9 acts as an inhibitory molecule, regulating the expansion and development of iNKT cells and innate-like CD8+ T cells. The regulatory role of Ly9 is still largely unclear, but it may represent an important therapeutic target for diseases in which iNKT cell numbers are relevant.
This study also identified an additional LY9-inhibitory gene, LY9E. LY9E, a gene encoding a negative regulator of the development and homeostasis of innate-like CD8+, iNKT cells, and innate-like B cells, regulates iNKT cell development and homeostasis. The role of LY9E is primarily determined by its role in controlling the differentiation of iNKT cells.
In mice lacking Ly9, iNKT cells are under-expressed, and they show marked differences in their subsets. Ly9-deficient mice have an expanded population of CD8 SP thymocytes, but a marked reduction in the number of innate-like CD8+ T cells and reduced activation in peripheral blood lymphocytes.
The SLAM-SAP-FynT pathway is essential for the positive selection of hemopoietic selecting cells. Hemopoietic cells have weak affinity for TCR coreceptors and antigen-MHC-derived signals. Therefore, a positive signal from SAP-dependent SLAM-SAP-FynT pathway may be required for these cells to differentiate into iNKT cells.
However, the role of SAP in iNKT cell development remains unclear. Currently, it is not known whether SAP negatively regulates the development of iNKT cells, although conditionally targeted mice can selectively ablate the expression of SAP in T and B cells.
Anti-Ly9 antibody treatment can inhibit iNKT cell differentiation by reducing their number and inhibiting their cytokine production. Anti-Ly9 antibodies were used to inhibit IL-4 production. Furthermore, anti-Ly9 treatment reduced spleen iNKT cell numbers by approximately 50%. This suggests that anti-Ly9 targeting may represent a promising therapeutic strategy for iNKT cell differentiation.
In contrast, mice lacking the SLAM and Ly108 receptors showed a 50%-70% reduction in the number of NKT cells in the thymus, spleen, and liver. This means that both SLAM and Ly108 receptors are essential in the development of iNKT and NKT cells.
In addition to its role in regulating immune system physiology, LY9 is also essential for regulating a subset of gd T cells. Inflammatory response inhibits the expression of these molecules, which maintain a subset of gd T cells. These abnormal T cells lead to an increased number of inflammatory gd T cells, predisposing the tissue to chronic inflammation.
Interestingly, LY9 has also been found to regulate metabolic activity in naive T cells. Increasing LDL concentration reduced the metabolic activities of Vg9+Vd2+ T cells, including the production of cellular ATP, secretor cytokines, and mitochondrial mass. This suggests that in obese individuals with high LDL levels, circulating LDL-related IL-23+ T cells are impaired in their ability to function properly. These results point to the possible role of LY9 in obesity and other metabolic disorders.
The LY9 receptor is a crucial component of autoantibody development. Lack of Ly9 receptor results in progressive development of autoantibodies without epistatic interactions. This mechanism was used in the development of Ly9-deficient mice, which lack the LY9 receptor. These mice display impaired autoantibody development. Further studies are needed to clarify the mechanism of Ly9 protection. Although the mechanisms involved are not clear, Ly9 may provide a useful target for the study of autoimmunity and may help build a rational road map towards understanding the causes of SLE syndrome.
The LY9 gene product is a unique human leukocyte cell surface marker that is related to the mouse Ly-9. It is a 2.6 kb messenger RNA expressed in lymph nodes, spleen, and thymus. Mice lacking Ly-9 proliferate poorly and produce very little IL-2 after suboptimal stimulation with anti-CD3 in vitro. The BXH strain contains up to 46% genetic variation due to the segregation of Ly-9.
In a new study, Ly9 was designated as a novel lymphocyte surface alloantigen. Flow microfluorescence can detect Ly 9 as an extra-specificity molecule in sera, whereas immunofluorescence quantification shows reduced expression and co-dominant expression. These studies suggest that the LY9 gene is essential for the survival of cancer cells. They may also be useful for diagnosis.
LY9 gene ablation affects peripheral B and T cell subsets implicated in autoimmunity. In a study of Ly9-/-(BALB/c.129) mice, there was a slight increase in CD4+ T and iNKT subsets. However, the majority of alterations were observed in B-cell subsets, specifically Transitional T1-B cells.
Recent studies show that Ly9 also is involved in humoral autoimmune responses. In mice that lack Ly9, autoantibodies (ANA) were detected in their serum. Ly9-/ mice had significantly higher ANA titers than wt mice. While Ly9 is not essential for autoimmunity, it is implicated in the initiation of autoimmunity. These findings suggest that Ly9 is a non-redundant cell surface receptor that inhibits autoantibody responses.
PMID: 10970093 by Tovar V., et al. Gene structure of the mouse leukocyte cell surface molecule Ly9.
PMID: 8537117 by Sandrin M.S., et al. Isolation and characterization of cDNA clones for Humly9: the human homologue of mouse Ly9.