Mouse GITR Ligand ELISA kit (DEIA5425)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
96T
Sample
serum, plasma, cell culture supernatants
Species Reactivity
Mouse
Intended Use
The Mouse GITR Ligand (glucocorticoid induced tumor necrosis factor receptor family related gene ligand) ELISA (Enzyme-Linked Immunosorbent Assay) kit is an in vitro enzyme-linked immunosorbent assay for the quantitative measurement of Mouse GITR Ligand in serum, plasma and cell culture supernatants.
Contents of Kit
1. GITR Ligand Microplate
2. Wash Buffer Concentrate
3. Standards
4. Assay Diluent A
5. Assay Diluent B
6. Detection Antibody GITR Ligand
7. HRP-Streptavidin Concentrate
8. TMB One-Step Substrate Reagent
9. Stop Solution
Storage
May be stored for up to 6 months at 2-8°C from the date of shipment. Standard (recombinant protein) should be stored at -20°C or -80°C (recommended at -80°C) after reconstitution. please download the following document on our website.
Sensitivity
4 pg/mL

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References


Rhinovirus infection induces distinct transcriptome profiles in polarized human macrophages

PHYSIOLOGICAL GENOMICS

Authors: Rajput, Charu; Walsh, Megan P.; Eder, Breanna N.; Metitiri, Ediri E.; Popova, Antonia P.; Hershenson, Marc B.

Infections with rhinovirus (RV) cause asthma exacerbations. Recent studies suggest that macrophages play a role in asthmatic airway inflammation and the innate immune response to RV infection. Macrophages exhibit phenotypes based on surface markers and gene expression. We hypothesized that macrophage polarization state alters gene expression in response to RV infection. Cells were derived from human peripheral blood derived monocytes. M1 and M2 polarization was carried out by using IFN-gamma and IL-4, respectively, and RNA was extracted for Affymetrix Human Gene ST2.1 exon arrays. Selected genes were validated by quantitative (q)PCR. Treatment of nonactivated (M0) macrophages with IFN-gamma and IL-4 induced the expression of 252 and 153 distinct genes, respectively, including previously-identified M1 and M2 markers. RV infection of M0 macrophages induced upregulation of 232 genes; pathway analysis showed significant overrepresentation of genes involved in IFN-alpha/beta signaling and cytokine signaling in the immune system. RV infection induced differential expression of 195 distinct genes in M1-like macrophages but only seven distinct genes in M2-like-polarized cells. In a secondary analysis. comparison between M0-, RV-infected, and M1-like-polarized, RV-infected macrophages revealed differential expression of 227 genes including those associated with asthma and its exacerbation. qPCR demonstrated increased expression of CCL8, CXCL10, TNFSF10, TNFSF18, IL6, NOD2, and GSDMD and reduced expression of VNN1, AGO1, and AGO2. Together, these data show that, in contrast to M2-like-polarized macrophages, gene expression of M1-like macrophages is highly regulated by RV.

Glucocorticoid-induced TNF receptor family- related protein ligand regulates the migration of monocytes to the inflamed intestine

FASEB JOURNAL

Authors: Liao, Gongxian; van Driel, Boaz; Magelky, Erica; O'Keeffe, Michael S.; Malefyt, Rene de Waal; Engel, Pablo; Herzog, Roland W.; Mizoguchi, Emiko; Bhan, Atul K.; Terhorst, Cox

Glucocorticoid-induced TNF receptor family-related protein (GITR) regulates the function of both T cells and antigen-presenting cells (APCs), while the function of GITR ligand (GITR-L) is largely unknown. Here we evaluate the role of GITR-L, whose expression is restricted to APCs, in the development of enterocolitis. On injecting naive CD4(+) T cells, GITR-L(-/-)Rag(-/-) mice develop a markedly milder colitis than Rag(-/-) mice, which correlates with a 50% reduction of Ly6C(+)CD11b(+)MHCII(+) macrophages in the lamina propria and mesenteric lymph nodes. The same result was observed in CD40-induced acute colitis and during peritonitis, suggesting an altered monocyte migration. In line with these observations, the number of nondifferentiated monocytes was approximately 3-fold higher in the spleen of GITR-L(-/-)Rag(-/-) mice than in Rag(-/-) mice after CD40 induction. Consistent with the dynamic change in the formation of an active angiotensin II type 1 receptor (AT1) dimer in GITR-L-/- splenic monocytes during intestinal inflammation, the migratory capability of splenic monocytes from GITR-L-deficient mice was impaired in an in vitro transwell migration assay. Conversely, GITR-L reduces the number of splenic Ly6C(hi) monocytes, concomitantly with an increase in AT1 dimers. We conclude that GITR-L regulates the number of proinflammatory macrophages in sites of inflammation by controlling the egress of monocytes from the splenic reservoir.Liao, G., van Driel, B., Magelky, E., O'Keeffe, M. S., de Waal Malefyt, R., Engel, P., Herzog, R. W., Mizoguchi, E., Bhan, A. K., Terhorst, C. Glucocorticoid-induced TNF receptor family-related protein ligand regulates the migration of monocytes to the inflamed intestine.

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