Human Chemokine (C-C motif) Ligand 5, CCL5 ELISA Kit (CKERS-CCL5-197H)

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

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serum, plasma, other biological fluids
Species Reactivity
Intended Use
This assay is a sandwich Enzyme Linked-Immuno-Sorbent Assay (ELISA). It is developed for quantitative measurement of Human CCL5 in serum, plasma and other biological fluids.
Contents of Kit
1. Human CCL5 Microplate: polystyrene microplate coated with a monoclonal antibody against Human CCL5;
2. Standard (freeze dried): 1,000 pg/mL, 2 vials;
3. Biotin-antibody (100x): 2 vials;
4. HRP-avidin (100x): 2 vials;
5. Reagent Diluent: 25 mL, 2 vials;
6. TMB Substrate: 12 mL, 1 vial;
7. TMB Stop Solution: 1 vial;
8. Wash Buffer (20x): 30 mL, 1 vial;
9. Microtiter plate sealers: 3 sheets.
Unopened Kit: Store at 2-8°C. Do not use past kit expiration date.
Opened/Reconstituted Reagents: Standard or Sample Diluent; Biotin-antibody Diluent; HRP-avidin Diluent; TMB Substrate; Wash Buffer; TMB Stop Solution. The above mentioned reagents should be stored for up to 1 month at 2-8°C.
Microplate Wells: Return unused wells to the foil pouch containing the desiccant pack, reseal along entire edge of zip-seal. May be stored for up to 1 month at 2-8°C.
Detection Rage: 15.625-1,000 pg/mL.
Detection Limit: The minimum detectable dose of Human CCL5 is typically less than 7 pg/mL.


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Anti-Inflammatory Activity of Miodesin (TM): Modulation of Inflammatory Markers and Epigenetic Evidence


Authors: Oliveira, Carlos Rocha; Vieira, Rodolfo Paula

Purpose. To investigate the effects of a combined herbal medicine Miodesin (TM) on the inflammatory response of key cells involved in the acute and chronic inflammatory processes as well as the possible epigenetic involvement. Methods. After the establishment of the IC50 dose, the chondrocyte, keratinocyte, and macrophage cell lines were pretreated for 2 hours with Miodesin (TM) (200 mu g/mL) and stimulated with LPS (1 mu g/mL) for 24 hours. The supernatant was used to measure the levels of cytokines (IL-1 beta, IL-6, IL-8, and TNF-alpha) and chemokines (CCL2, CCL3, and CCL5), and the cells were used to extract the mRNA for the transcription factor (NF-kappa beta), inflammatory enzymes (COX-1, COX-2, PLA2, and iNOS), and chemokines (CCL2, CCL3, and CCL5). Results. Miodesin (TM) inhibited the release of LPS-induced cytokines (IL-1 beta, IL-6, IL-8, and TNF-alpha; p<0.01) and chemokines (CCL2, CCL3, and CCL5; p<0.01) and the expression of the transcription factor (NF-kappa beta; p<0.01), inflammatory enzymes (COX-1, COX-2, PLA2, iNOS; p<0.01), and chemokines (CCL2, CCL3, and CCL5; p<0.01). In addition, the evaluation of epigenetic mechanism revealed that Miodesin (TM) did not induce changes in DNA methylation, assuring the genetic safeness of the compound in terms of the inflammatory response. Conclusions. Miodesin (TM) presents anti-inflammatory properties, inhibiting hyperactivation of chondrocytes, keratinocytes, and macrophages, involving epigenetics in such effects.

Midkine activation of CD8(+) T cells establishes a neuron-immune-cancer axis responsible for low-grade glioma growth


Authors: Guo, Xiaofan; Pan, Yuan; Xiong, Min; Sanapala, Shilpa; Anastasaki, Corina; Cobb, Olivia; Dahiya, Sonika; Gutmann, David H.

Brain tumors (gliomas) are heterogeneous cellular ecosystems, where non-neoplastic monocytic cells have emerged as key regulators of tumor maintenance and progression. However, relative to macrophages/microglia, comparatively less is known about the roles of neurons and T cells in glioma pathobiology. Herein, we leverage genetically engineered mouse models and human biospecimens to define the axis in which neurons, T cells, and microglia interact to govern Neurofibromatosis-1 (NF1) low-grade glioma (LGG) growth. NF1-mutant human and mouse brain neurons elaborate midkine to activate naive CD8(+) T cells to produce Ccl4, which induces microglia to produce a key LGG growth factor (Ccl5) critical for LGG stem cell survival. Importantly, increased CCL5 expression is associated with reduced survival in patients with LGG. The elucidation of the critical intercellular dependencies that constitute the LGG neuroimmune axis provides insights into the role of neurons and immune cells in controlling glioma growth, relevant to future therapeutic targeting. The role of neurons and T cells in glioma progression remains poorly understood. Here the authors show that midkine-dependent activation of a neuron-T cell-microglia axis promotes the growth of optic pathway gliomas.

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