Anti-hTLR5-IgA

Human TLR5 Detection and Neutralizing antibody - Monoclonal Human IgA2 (Q2G4)

Anti-hTLR5-IgA2 is a chimeric monoclonal antibody specific for humanToll-like receptor 5 (TLR5). It was generated by combining the constant domains of the human IgA molecule with murine variable regions.

It was produced in Chinese hamster ovary (CHO) cells and purified by affinity chromatography.

Anti-hTLR5-IgA2 has been selected for its ability to efficiently neutralize the biological activity of TLR5. The neutralizing activity  was determined using HEK-Blue™ TLR5 Cells.

It was found to be significantly higher than the neutralizing activity of the corresponding IgG isotype.

Specifications

Clonality: Monoclonal antibody

Specificity: Human TLR5

Clone: Q2G4

Isotype: Human IgA2, kappa

Control: Human IgA2 Control

Source: CHO cells

Formulation: 0.2 μm filtered solution in TRIS with glycine, saccharose, and stabilizing agents

Tested applications: Neutralizing human TLR5-induced cellular activation. This antibody can also be used for detection using flow cytometry

Contents

• 100 μg purified anti-hTLR5-IgA antibody, provided azide-free and lyophilized.

Product is shipped at room temperature.

Upon receipt, store lyophilized antibody at -20 °C.

Description

Toll-like receptors (TLRs) play a critical role in early innate immunity to invading pathogens by sensing microorganisms. These evolutionarily conserved receptors recognize highly conserved structural motifs only expressed by microbial pathogens, called pathogen-associated microbial patterns (PAMPs). Stimulation of TLRs by PAMPs initiates a signaling cascade leading to the secretion of proinflammatory cytokines following NF-κB activation. To date ten human and twelve murine TLRs have been characterized, TLR1 to TLR10 in humans, and TLR1 to TLR9, TLR11, TLR12, and TLR13 in mice, the homolog of TLR10 being a pseudogene.

TLR5 recognizes flagellin from both Gram-positive and Gram-negative bacteria. Activation of the receptor stimulates the production of proinflammatory cytokines, such as TNF-α, through signaling via the adaptor protein MyD88 and the serine kinase IRAK [1, 2]. TLR5 can generate a proinflammatory signal as a homodimer suggesting that it might be the only TLR participating in flagellin recognition [2]. However, TLR5 may require the presence of a co-receptor or adaptor molecule for efficient ligand recognition and/or signaling [3].

1. Gewirtz A.T. et al., 2001. Cutting edge: bacterial flagellin activates basolaterally expressed TLR5 to induce epithelial proinflammatory gene expression. J Immunol, 167(4):1882-5.
2. Hayashi F. et al., 2001. The innate immune response to bacterial flagellin is mediated by Toll-like receptor 5. Nature, 410(6832):1099-103.
3. Tallant T. et al., 2004. Flagellin acting via TLR5 is the major activator of key signaling pathways leading to NF-kappa B and proinflammatory gene program activation in intestinal epithelial cells. BMC Microbiol. 4(1):33.