TLR3 in Human Eosinophils: Functional Effects and Decreased Expression during Allergic Rhinitis

Månsson, Alf; Fransson, Mattias; Adner, Mikael; Benson, Mikael; Uddman, Rolf; Björnsson, Sven; Cardell, Lars-Olaf

doi:10.1159/000236001

Cited by 38 publications

(28 citation statements)

References 74 publications

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“…These 17 SNPs comprise 2 on TLR1, 4 on TLR2, 2 on TLR4, 3 on TLR6, 1 on TLR7, 2 on TLR8, 1 on TLR9, and 2 on TLR10. Although expressions of TLR3 and TLR5 have been linked with allergic rhinitis34 and asthma,36 none of the SNPs on TLR3 and TLR5 has been shown to be associated with allergic diseases.…”

Section: Tlr Snps and Allergic Diseasesmentioning

confidence: 99%

Allergic rhinitis and genetic components: focus on Toll-like receptors (TLRs) gene polymorphism

Gao

Rennie²

2010

TACG

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Allergic rhinitis represents a global health issue affecting 10% to 25% of the population worldwide. Over the years, studies have found that allergic diseases, including allergic rhinitis, are associated with immunological responses to antigens driven by a Th2-mediated immune response. Because Toll-like receptors (TLRs) are involved in both innate and adaptive immune responses to a broad variety of antigens, the association between polymorphisms of TLRs and allergic diseases has been the focus in many animal and human studies. Although the etiology of allergic rhinitis is still unknown, extensive research over the years has confirmed that the underlying causes of allergic diseases are due to many genetic and environmental factors, along with the interactions among them, which include gene–environment, gene–gene, and environment–environment interactions. Currently, there is great inconsistency among studies mainly due to differences in genetic background and unique gene–environment interactions. This paper reviews studies focusing on the association between TLR polymorphisms and allergic diseases, including allergic rhinitis, which would help researchers better understand the role of TLR polymorphisms in the development of allergic rhinitis, and ultimately lead to more efficient therapeutic interventions being developed.

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Section: Tlr Snps and Allergic Diseasesmentioning

confidence: 99%

Allergic rhinitis and genetic components: focus on Toll-like receptors (TLRs) gene polymorphism

Gao

Rennie²

2010

TACG

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“…Furthermore, Mansson and colleagues stated that expression of TLR7 and TLR9 was the same between healthy and atopic patients. However, upon in vitro TLR stimulation with R-837 (TLR7) or CpG (TLR9), eosinophils from atopic patients had increased cytokine production and granule protein secretion compared to those from healthy patients [17]. These data suggest that important differences exist between these two conditions (atopic vs. healthy status) and immunological environments [17].…”

Section: Pathogen Recognition By Eosinophilsmentioning

confidence: 99%

“…However, upon in vitro TLR stimulation with R-837 (TLR7) or CpG (TLR9), eosinophils from atopic patients had increased cytokine production and granule protein secretion compared to those from healthy patients [17]. These data suggest that important differences exist between these two conditions (atopic vs. healthy status) and immunological environments [17]. It is important to consider these observations, as they may explain some of the discrepancies regarding specific TLR expression and subsequent activation of eosinophils.…”

Section: Pathogen Recognition By Eosinophilsmentioning

confidence: 99%

“…Several studies found that human eosinophils constitutively express mRNA for TLR7, TLR8, and TLR9 and cell surface receptors for TLR7 and TLR8. These receptors are detectable by flow cytometry, though surface expression levels were lower in eosinophils than in neutrophils [15, 17, 18]. Additionally, these receptors are functional as TLR9 stimulation using CpG induced secretion of EDN from eosinophils, and enhanced chemotaxis [17].…”

Section: Pathogen Recognition By Eosinophilsmentioning

confidence: 99%

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The Role of Eosinophils in Non-Parasitic Infections

Linch¹,

Gold²

2011

EMIDDT

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Eosinophils are a subset of leukocytes the traditionally associated with Th2-related diseases and helminth infections. However, accumulating evidence suggests that eosinophils play a more prominent role in the immune response to bacterial and viral pathogens than previously realized. Specifically, eosinophils possess antimicrobial properties against a broad range of pathogens, and release specific and secondary granules as a result of pathogen recognition. Pathogen recognition is accomplished through expression of Toll-like receptors, as well as other surface and intracellular receptors expressed by the eosinophil. Interestingly, specific killing mechanisms employed by each granule protein differ based on pathogen recognition, but ultimately release of eosinophil granules leads to direct killing of many different pathogens. The precise mechanisms of killing by granule proteins and the circumstances in which specific proteins are secreted are only now being determined. Future efforts to understand these mechanisms may lead toward clinical use of granule proteins as antimicrobial agents in humans, in addition to revealing implications regarding the use of eosinophil-depleting therapies for allergic disorders. This review will summarize the literature to date regarding the role of eosinophils in non-parasitic infections.

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“…Szczeklik1 has hypothesized that AERD develops as the result of chronic viral infection. Recently, it has been shown that eosinophils activated via Toll-like receptor 3 (TLR3) might be more able to recruit leukocytes to sites of inflammation, and that eosinophils might function as a link between viral infection and exacerbation of allergic disease 2. Viral respiratory infections have been suggested to contribute to allergic sensitization and development of asthma, and in subjects with already established asthma, they are known to exacerbate the allergic disease 3.…”

Section: Introductionmentioning

confidence: 99%

Role ofToll-like Receptor 3Variants in Aspirin-Exacerbated Respiratory Disease

Palikhe

Kim

et al. 2011

Allergy Asthma Immunol Res

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PurposeAlthough the mechanism of virus-induced, aspirin-exacerbated respiratory disease (AERD) is not known fully, direct activation of viral components through Toll-like receptor 3 (TLR3) has been suggested. TLR3 recognizes double-stranded RNA (dsRNA), and activates nuclear factor-κB and increases interferon-γ, which signals other cells to induce airway inflammation in asthma. Considering the association of TLR3 in viral infections and AERD, we investigated whether promoter and non-synonymous variants of TLR3 were associated with AERD.MethodsThe three study groups, 203 with AERD, 254 with aspirin-tolerant asthma (ATA), and 274 normal healthy controls (NC) were recruited from Ajou University Hospital, Korea. Two polymorphisms, -299698G>T and 293391G>A [Leu412Phe], were genotyped using primer extension methods.ResultsGenetic associations were examined between two genetic polymorphisms of TLR3 (-299698G>T and 293391G>A [Leu412Phe]) in the three study groups. AERD patients that carried the GG genotype of 293391G>A showed a significantly lower frequency compared with ATA in both co-dominant (P=0.025) and dominant models (P=0.036). Similarly, in the minor allele frequency, the A allele was significantly higher (P=0.023) in AERD compared with ATA for this polymorphism. AERD patients who carried HT2 [GA] showed a significantly higher frequency than other haplotypes in co-dominant (P=0.02) and recessive (P=0.026) models.ConclusionsOur findings suggest that the -299698G>T and 293391G>A [Leu412Phe] polymorphisms of the TLR3 gene are associated with the AERD phenotype.

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TLR3 in Human Eosinophils: Functional Effects and Decreased Expression during Allergic Rhinitis

Cited by 38 publications

References 74 publications

Allergic rhinitis and genetic components: focus on Toll-like receptors (TLRs) gene polymorphism

Allergic rhinitis and genetic components: focus on Toll-like receptors (TLRs) gene polymorphism

The Role of Eosinophils in Non-Parasitic Infections

Role ofToll-like Receptor 3Variants in Aspirin-Exacerbated Respiratory Disease

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