Anti-hTLR5-IgA

Anti-hTLR5-IgA 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.

Anti-hTLR5-IgA has been selected for its ability to efficiently neutralize the biological activity of TLR5. The neutralizing activity of this IgA antibody 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

Applications: Neutralizing human TLR5-induced cellular activation. This antibody can also be used for flow cytometry.

Specificity: Human TLR5

Clone: Q2G4

Isotype: Human IgA2

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

Contents

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

Product is shipped at room temperature.

Store lyophilized antibody at -20 °C.

Lyophilized product is stable for at least 1 year.

Description

Toll-like receptors (TLRs) play a critical role in early innate immunity to invading pathogens by sensing microorganisms. These evolutionary 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 AT. 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.