Immunoglobulin-like transcript 4 (ILT-4) is a crucial immunomodulatory receptor predominantly expressed on myeloid cells, including dendritic cells, macrophages, and monocytes. It plays a significant role in the regulation of the immune response, particularly in the maintenance of immune tolerance and the modulation of antigen presentation. ILT-4 achieves these functions by binding to its ligands, including major histocompatibility complex (MHC) class I molecules, which leads to the inhibition of cell-mediated immune responses. Through its interactions, ILT-4 is involved in the suppression of T-cell activation and the promotion of tolerance by influencing the cytokine production profiles of immune cells. The receptor's activity is critical for preventing overactive immune responses that could result in autoimmunity or tissue damage, highlighting its role in maintaining immune homeostasis.
The inhibition of ILT-4 involves mechanisms that decrease its ability to mediate immune suppression, thereby potentially enhancing immune responses. This can be achieved through various molecular interactions that disrupt the engagement of ILT-4 with its ligands or interfere with its signal transduction pathways. For instance, blocking the binding sites on ILT-4 that interact with MHC class I molecules can prevent the receptor from exerting its immunosuppressive effects. Additionally, alterations in the expression levels of ILT-4, either through genetic regulation or post-translational modifications, can influence its activity and the extent of its inhibitory functions on the immune response. Such mechanisms of inhibition are not only pivotal for understanding how immune tolerance is regulated but also for elucidating the pathways through which the immune system can be modulated. By focusing on the direct interactions and regulatory processes that control ILT-4 activity, researchers can gain insight into the complex network of signals that govern immune tolerance and the potential for manipulating these pathways to address dysregulated immune responses.
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| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Sunitinib, Free Base | 557795-19-4 | sc-396319 sc-396319A | 500 mg 5 g | $153.00 $938.00 | 5 | |
Sunitinib inhibits ILT-4 indirectly by targeting the VEGF and PDGF pathways. It suppresses receptor tyrosine kinases involved in these pathways, leading to downstream effects that modulate ILT-4 expression and function, ultimately inhibiting its role in immune regulation. | ||||||
Dasatinib | 302962-49-8 | sc-358114 sc-358114A | 25 mg 1 g | $70.00 $145.00 | 51 | |
Dasatinib, a Src kinase inhibitor, indirectly inhibits ILT-4 by disrupting the Src signaling pathway. Src kinase plays a role in ILT-4 regulation, and Dasatinib's inhibition alters the phosphorylation status of Src, influencing ILT-4 expression and function in immune modulation. | ||||||
Rapamycin | 53123-88-9 | sc-3504 sc-3504A sc-3504B | 1 mg 5 mg 25 mg | $63.00 $158.00 $326.00 | 233 | |
Rapamycin inhibits ILT-4 indirectly through mTOR pathway modulation. By inhibiting mTOR, Rapamycin disrupts downstream signaling cascades that influence ILT-4 expression and function, providing an indirect inhibition of ILT-4 in immune regulation. | ||||||
LY 294002 | 154447-36-6 | sc-201426 sc-201426A | 5 mg 25 mg | $123.00 $400.00 | 148 | |
LY294002, a PI3K inhibitor, indirectly inhibits ILT-4 by disrupting the PI3K-Akt pathway. Inhibition of PI3K influences Akt signaling, altering ILT-4 expression and function in immune modulation processes. | ||||||
Syk Inhibitor IV, BAY 61-3606 HCl | 732983-37-8 | sc-202351 | 2 mg | $327.00 | 25 | |
BAY 61-3606, a Syk inhibitor, indirectly inhibits ILT-4 by disrupting the Syk signaling pathway. Syk is involved in ILT-4 regulation, and BAY 61-3606's inhibition alters the phosphorylation status of Syk, influencing ILT-4 expression and function in immune modulation. | ||||||
Bortezomib | 179324-69-7 | sc-217785 sc-217785A | 2.5 mg 25 mg | $135.00 $1085.00 | 115 | |
Bortezomib inhibits ILT-4 indirectly through NF-κB pathway modulation. By inhibiting the proteasome, Bortezomib influences NF-κB signaling, which in turn modulates ILT-4 expression and function, providing an indirect inhibition of ILT-4 in immune regulation. | ||||||
Ruxolitinib | 941678-49-5 | sc-364729 sc-364729A sc-364729A-CW | 5 mg 25 mg 25 mg | $251.00 $500.00 $547.00 | 16 | |
Ruxolitinib inhibits ILT-4 indirectly by targeting the JAK-STAT pathway. It inhibits JAK1 and JAK2, leading to downstream effects that modulate ILT-4 expression and function, providing an indirect inhibition in immune regulation. | ||||||
SB 203580 | 152121-47-6 | sc-3533 sc-3533A | 1 mg 5 mg | $90.00 $349.00 | 284 | |
SB203580, a p38 MAPK inhibitor, indirectly inhibits ILT-4 by disrupting the p38 MAPK pathway. Inhibition of p38 MAPK influences downstream signaling cascades that modulate ILT-4 expression and function, providing an indirect inhibition in immune regulation. | ||||||
Imatinib | 152459-95-5 | sc-267106 sc-267106A sc-267106B | 10 mg 100 mg 1 g | $26.00 $119.00 $213.00 | 27 | |
Imatinib inhibits ILT-4 indirectly by targeting the PDGF and c-Kit pathways. It suppresses receptor tyrosine kinases involved in these pathways, leading to downstream effects that modulate ILT-4 expression and function, ultimately inhibiting its role in immune regulation. | ||||||
Selumetinib | 606143-52-6 | sc-364613 sc-364613A sc-364613B sc-364613C sc-364613D | 5 mg 10 mg 100 mg 500 mg 1 g | $29.00 $82.00 $420.00 $1897.00 $3021.00 | 5 | |
Selumetinib, a MEK inhibitor, indirectly inhibits ILT-4 by disrupting the MAPK pathway. It inhibits MEK1/2, leading to downstream effects that modulate ILT-4 expression and function, providing an indirect inhibition in immune regulation. | ||||||