Products from BPS Bioscience require a minimum order value above 400€Application: Screen and characterize modulators of IL-5 signaling.
Background: IL-5 (interleukin-5) is a pro-inflammatory protein that functions as an intermediary cytokine in the T
H2 (T helper 2) cells response in asthma and other eosinophilic allergic diseases. IL-5 is produced by T
H2 cells and ILC2 (group 2 innate lymphoid cells) cells in response to stimulation by alarmins such as TSLP (thymic stromal lymphopoietin) or IL-33, which initiate the inflammatory cascade. IL-5 functions by promoting eosinophil maturation, activation, and migration into target tissues. It binds to the IL-5 specific cell surface receptor IL-5RA (IL-5 receptor alpha) and further recruits the common beta chain receptor (CSF2RB) to initiate downstream signaling through JAK1/2 (Janus kinase 1/2) and STAT5. Activated eosinophils contribute to airway damage through degranulation, resulting in the release of pro-inflammatory cytokines and enzymatic mediators contributing to local inflammation and tissue damage.IL-5 signaling plays a critical role in allergic and eosinophilic asthma subtypes and has been an active area for drug discovery. Antibodies targeting both IL-5 ligand and IL-5 Receptor (IL-5RA) are FDA (Food and Drug Administration) approved for the treatment of severe eosinophilic asthma and other eosinophilic conditions. These antibodies function by neutralizing IL-5-mediated signaling in eosinophils. Additionally, IL-5RA targeting antibodies and CAR (chimeric antigen receptor)-T cells can induce immune-mediated cytotoxicity of IL-5RA-expressing cells, including eosinophils through ADCC (antibody-dependent cellular cytotoxicity) and CAR-T cell mediated killing respectively.
Description: The IL-5 Responsive Luciferase Reporter Ba/F3 Cell Line is a murine Ba/F3 cell line engineered to express both human IL-5RA (IL-5 receptor alpha, also known as CD125) (NM_175726.4) and human CSF2RB (common receptor beta chain also known as IL5RB or CD131) (NM_000395.3), separated by a self-cleaving P2A peptide. The construct was delivered by lentiviral transduction of the STAT5 Luciferase Reporter Ba/F3 Cell Line (#79772), which expresses a firefly luciferase reporter driven by the STAT5 (signal transducer and activator of transcription 5) response elements located upstream of the minimal TATA promoter. After activation by IL-5, the endogenous transcription factor STAT5 binds to the response elements, inducing transcription of the luciferase reporter.This cell line has been validated to respond to IL-5. Additional functional validation demonstrates that IL-5-induced luciferase activity can be inhibited by either anti-IL-5 or anti-IL-5R neutralizing antibodies.
Figure 1: Illustration of the mechanism of IL-5 Luciferase Reporter Ba/F3 Cell Line. IL-5 binds to IL-5 receptor alpha subunit, facilitating its interaction with the common receptor beta chain (CSF2RB), and activating downstream JAK1/2 (Janus kinase 1/2) tyrosine kinases, which phosphorylate the transcription factor STAT5 (signal transducer and activator of transcription 5). STAT5 phosphorylation triggers the formation of a homodimer and translocation to the nucleus, where it can activate the transcription of the Firefly luciferase reporter driven by STAT5 response elements present in the promoter.Interested in screening and profiling inhibitors or blocking antibodies of IL-5 in a cell culture assay without the need to purchase and license the cell line? Check out our
Cell Signaling Pathway Screening.Genbank: NM_175726.4, NM_000395.3
Host Cell Line: Ba/F3, mouse IL-3-dependent pro-B cell line, suspension.
Mycoplasma Testing: The cell line has been screened to confirm the absence of Mycoplasma species.
Storage Stability: Cells are shipped in dry ice and should immediately be thawed or stored in liquid nitrogen upon receipt. Do not use a -80°C freezer for long term storage.
Supplied As: Each vial contains ˃1 X 10
6 cells in 1 ml of Cell Freezing Medium (BPS Bioscience #79796)
Warnings: Avoid freeze/thaw cycles.
Biosafety Level: BSL-1
References:
Kim J-E., et al., 2021 Front. Immunol. 11:593748.
Lawrence M., et al., 2019 Ann of Allergy, Asthma Immunol 120(4): 376 – 381.
Matucci A., et al., 2019 Respir Med 160:105819.
Roufosse F., et al., 2018 Front. Med. 5:49.
Schleich F., et al., 2023 Eur Respir Rev 32(168): 220193.
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