Toll-like receptor 5 Antibodies

Toll-like receptor 5 (TLR5)

Participates in the innate immune response to microbial agents. Mediates detection of bacterial flagellins.

Acts via MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. .

Gene Information

Human
Gene Name:	TLR5
Uniprot:	O60602
Entrez:	7100

Family

Belongs to:
Toll-like receptor family

Alternative Names

MGC126430; MGC126431; SLEB1FLJ10052; TIL-3; TIL3Toll/interleukin-1 receptor-like protein 3; TLR5; toll-like receptor 5

Molecular Weight

Mass (kDA):
97.834 kDA

Genomic Context

Human
Location:	1q41
Sequence:	1; NC_000001.11 (223108401..223143281, complement)

Tissue Specificity

Highly expressed in ovary and in peripheral blood leukocytes, especially in monocytes, less in CD11c+ immature dendritic cells. Also detected in prostate and testis.

Subcellular Localizations

Cell membrane; Single-pass type I membrane protein.

Diseases

• Inflammation
• Innate Immune Response
• Salmonella Infections
• Infective Disorder
• Inflammatory Response
• Pneumonia
• Bacterial Infections
• Malignant Neoplasms
• Neoplasms
• Colitis
• Systemic Infection
• Intestinal Diseases
• Influenza

• Ulcer
• Pseudomonas Infections
• Crohn Disease
• Inflammatory Bowel Diseases
• Salmonella Infections, Animal
• Tissue Adhesions
• Fibrosis

Pathways

• Immune Response
• Secretion
• Innate Immune Response
• Cytokine Production
• Pathogenesis
• Inflammatory Response
• Cell Activation
• Cell Proliferation
• Localization
• Adaptive Immune Response
• Phagocytosis
• Chemokine Production
• Virulence

• Chemokine Secretion
• Aging
• Cell Death
• Reverse Transcription
• Transport
• Cytokine Secretion
• Response To Lipopolysaccharide

PTMs

• Phosphorylation
• Methylation
• Cleavage
• Glycosylation
• Biotinylation

• Nitration
• Reduction
• Dephosphorylation
• Acylation
• Myristoylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/TLR5

Best Uses Of The TLR5 Marker

There's a lot of talk about TLR5 signaling, and rightly so. But does it play a role in immune responses? No. It is evident that TLR5 isn't the main contributor to this response. In fact, it's a minor element. Continue reading to learn more about the most effective applications of TLR5 and what it can do.

This response doesn't play a major part in TLR5 signaling

TLR3 and TLR4 are bacteria-specific receptors which bind with endosomes. They form homo - or heterodimers, which trigger the signaling cascade. The downstream adaptor proteins TIRAP MyD88, TIRAP, and TRIF are involved in this signaling cascade. TLR activation triggers formation of the Myddosome, which is a component of IRAK1. TAK1 triggers MAPKs and transcription factors and TRAF6 promotes ECSIT ubiquitination.

Further research could clarify the roles of TLRs in the fight against cancer. Clarifying their roles in this response opens the way for new treatments and strategies to fight the disease. This will also assist scientists develop better anti-tumor vaccinations. This discovery could lead to more efficient treatments for cancer if it proves to be successful. In turn, the future of cancer research is much brighter.

Toll-like receptors on epithelial cells initiate flagellin-induced inflammatory signals. LPS hinders basolateral TLR5 activation while flagellin activates it. In spite of these distinctions, flagellin is unlikely not to be as widespread in the normal microbiota. This could be due to dissensitization of the epithelium to signaling processes initiated by bacterial flagellin.

Two human populations were examined and it was discovered that the presence of the TLR5 gene in the immune systems is linked to a higher chance of developing LD. People with CD are less likely than those with two WT alleles to develop the condition. So, TLR5 is not the main driver of this response. But it contributes to the susceptibility to LD. Keep reading if interested in knowing why it is so important to recognize this gene in your immune system.

Studies of TLR5 signaling have revealed that the TIR domains of adaptors are essential for activating this signaling pathway. Cell-based methods revealed that TLR5 has multiple roles in cellular function, including localization and protein modification. Recent studies have also revealed negative regulators of TLR signaling, which play an important role in an innate immune response. More research needs to be conducted in the near future to guarantee the health of patients.

Flagellin increases TLR5 expression in human cells The TLR5 gene is expressed in human cells. TLR5 was found to be the main TLR that activates the NF-kB. Previous studies have not been able to determine the presence of TLR5 in cells. This study has identified the type of cell that expresses the receptors by measuring flagellin protein levels and TLR5 levels. It is also possible that the activation of flagellin by NF-kB is dependent on TLR4 and TLR5 signaling.

TLR5 is a crucial component of the immune response to flagellin. However, it appears to play a bigger role than was previously thought. Flagellin is involved in CD and the pathogenic response. Although it is not clear if TLR5 alone is responsible for the CD-related phenotype, it is important to remember that pharmacological inhibition may be effective in preventing or treating CD.

The TLR5 protein is essential for TLR5 signalling. Its expression is lower in normal cervical epithelium squamous. However, cancerous cervical cells show higher levels of TLR5 expression. Understanding how this receptor regulates the NF-kB response is important for many ailments. It has been demonstrated to promote inflammatory responses through its role in HPV infection.

TLR5 is essential for LSK cell proliferation following flagellin stimulation. The treatment with flagellin stimulates LSK cell proliferation, which results in an increase of 10 times in the number of type 3 MPP and LTR cells. MPP3 cells that are stimulated by flagellin and co-transferred to bone marrow cells dramatically increased the survival rate of recipients of bone marrow transplants. They can also be administered to stop life-threatening neutropenia.

TLR5 is crucial in generating antibody responses against TIV. IgG1 and IgG2c antibody responses were significantly decreased in mice deficient in TLR5 expression. TLR5 is not necessary for the initiation of vaccine-induced TIV antibody responses, however. For non-hematopoietic cells TLR5 is not required. MyD88 isn't expressed in epithelial cells of mice that have been suppressed.

The induction of TLR5 was detected in blood and intestines of fish that have been stimulated with flagellin. The induction of IL-8 and TNF-a could be crucial in enhancing the fish's innate immunity. Understanding TLR5 and its role in this response may help us develop preventative measures in the coming years. Once TLR5 has been discovered to be essential for innate immunity, it could become a beneficial therapeutic target.