Association of three sets of high-affinity IgE receptor (FcepsilonR1) polymorphisms with aspirin-intolerant asthma

Palikhe, Nami Shrestha; Kim, Seung Hyun; Cho, Bo Young; Ye, Young-Min; Hur, Gyu Young; Park, Hae‐Sim

doi:10.1016/j.rmed.2008.03.017

Cited by 43 publications

(39 citation statements)

References 29 publications

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“…Highest serum IgE concentrations were observed in allergic subjects with FCER1A ¡344 TT|¡18483 CC & FCER1B ¡109 TT combined genotype, whereas the lowest levels were found in those with FCER1A ¡344 CT/CC|¡18483 AC/AA & FCER1B ¡109 TC/CC genotype group [21], which further expanded the previous studies on FCER1B ¡109 T>C genetic variant [28,29]. One study, conducted in Korean asthmatics with or without aspirin hypersensitivity, failed to replicate association between ¡344 C>T genetic variant and total serum IgE levels [24].…”

Section: Genetic Association Studies On Fcer1a Genementioning

confidence: 60%

“…An association between ¡344 T allele carrying status and higher prevalence of IgE-SEA antibodies was also observed in subjects with aspirin-intolerant asthma [24]. In the same group of patients, also ¡95 C>T polymorphism was associated with the prevalence of IgE-SEA and speciWc IgE against toxic shock syndrome toxin 1 (TSST-1) antibodies [24].…”

Section: Genetic Association Studies On Fcer1a Genementioning

confidence: 88%

“…This association with aspirin hypersensitivity failed, however, to replicate in Polish subjects [12,13] but inconsistent results could be explained by a diVerent selection criteria for the Polish group, which included subjects both with asthma and urticaria, and by ethnic diVerences in SNPs frequencies between Polish Caucasians and Korean East Asians [12][13][14][15]. Very recently, a lack of association between ¡344 C>T or ¡95 T>C SNP and asthma, irrespective of aspirin hypersensitivity, was reported in Koreans [24]. Several studies described a consistent genetic association between FCER1A variants, ¡344 C>T and ¡18483 A>C, and total serum IgE levels in allergic subjects [10,12,13,15,19,21].…”

Section: Genetic Association Studies On Fcer1a Genementioning

confidence: 99%

“…Very recently, several novel studies reported on unusual genetic variability of FCER1A and its relationship to atopy measures or allergic disorders in human [12][13][14][15][16][17][18][19][20][21][22][23][24]. The gene, though conserved in its coding region, shares some common 5Ј-untranslated region variants across several human populations.…”

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confidence: 99%

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Genetic variability of the high-affinity IgE receptor α-subunit (FcεRIα)

et al. 2008

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Our knowledge on the variability of FCER1A gene encoding for alpha-subunit of the high-affinity immunoglobulin E receptor (FcepsilonRI) that plays a central role in the pathogenesis of allergy and related disorders, has been recently much extended. Last findings from FCER1A mutational screening and genetic association studies, followed by functional analyses of the polymorphisms, are briefly summarized in this mini-review. The association between FCER1A gene variants and total serum IgE levels seems especially interesting and, supported by functional analyses of polymorphisms, may provide a rationale for pharmacogenetic studies on anti-IgE therapy that indirectly suppresses FcepsilonRI expression.

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Section: Genetic Association Studies On Fcer1a Genementioning

confidence: 60%

Section: Genetic Association Studies On Fcer1a Genementioning

confidence: 88%

Section: Genetic Association Studies On Fcer1a Genementioning

confidence: 99%

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confidence: 99%

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Genetic variability of the high-affinity IgE receptor α-subunit (FcεRIα)

et al. 2008

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“…TSLP could act through mast cell activation to stimulate the release of Th2 cytokines, which are implicated in the regulation of the arachidonic acid pathway [28,29]. Another potential mechanism of action could be through the TSLP-activated pSTAT5 pathway leading to FCER1G demethylation and FcεRI overexpression [30]; this mechanism could have a role in NSAID hypersensitivity, perhaps in conjunction with variation in the IgE receptor genes, which have been shown to be associated with this pathology, although results are mixed [31,32,33,34]. …”

Section: Discussionmentioning

confidence: 99%

Genetic Variants of Thymic Stromal Lymphopoietin in Nonsteroidal Anti-Inflammatory Drug-Induced Urticaria/Angioedema

Plaza-Serón

Blanca‐López²,

Pérez‐Sánchez³

et al. 2016

Int Arch Allergy Immunol

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Background: Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most frequent agents involved in hypersensitivity drug reactions, with NSAID-induced urticaria and/or angioedema (NIUA) being the most common entity. Mast cells are key players in NIUA and are activated by thymic stromal lymphopoietin (TSLP). This cytokine functions through recognition by its receptor, composed of IL7Rα (interleukin-7 receptor alpha) and TSLPR (TSLP receptor). These genes have been previously associated with other inflammatory diseases. Methods: We assessed the genetic association between single nucleotide polymorphisms (SNPs) in TSLP, IL7R and TSLPR and NIUA in Spanish individuals, using genotyped and imputed data. A total of 369 unrelated NIUA patients and 580 NSAID-tolerant control subjects were included, and 6 SNPs in TSLP, 6 in IL7R and 3 in TSLPR were genotyped. Further variants were imputed using Mach and the 1,000 Genomes Project (Phase 3) data. Association testing and statistical analyses were performed with Mach2dat and R. Results: A total of 139 SNPs were tested for association following quality control. Two SNPs in TSLP (rs1816678 and rs764917) showed a nominal association (p = 0.033 and 0.024, respectively) with NIUA, although these results were not statistically significant after correcting for multiple comparisons. Conclusions: Although TSLP, IL7R and TSLPR are important genes involved in the development of the inflammatory response, we found no significant genetic association with NIUA in our population for common SNPs in these genes.

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Adverse Immunological Reactions to Drugs

Ardern‐Jones

2016

Rook's Textbook of Dermatology, Ninth Edition

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Drug hypersensitivity reactions have been the subject of great interest to immunologists for more than half a century, yet the precise molecular pathways involved in their pathogenesis remain elusive. Significant recent advances include the discovery that abacavir directly binds the HLA‐B*5701 MHC peptide groove, thereby altering the repertoire of self‐peptides that can be expressed in the major histocompatibility complex (MHC). This induces T‐cell‐mediated inflammation and the hypersensitivity syndrome. Human leukocyte antigen (HLA) associations with severe cutaneous adverse reactions have so far been shown for six different drugs. However, the link between HLA association and clinical phenotype is confusing, with carbamazepine hypersensitivity associated with both HLA‐B*1502 and HLA‐A*3101. Genetic studies show that the former only predisposes to Stevens–Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN), yet the latter associates with exanthems, systemic hypersensitivity and SJS/TEN. In TEN, multiple molecular mechanisms of keratinocyte death have been postulated, but two predominate: (i) FasL up‐regulation and induction of Fas‐mediated keratinocyte cell death; and (ii) cytotoxic granulysin production by T, NK and NKT cells. Whether these act independently or synergistically remains to be established.

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Association of three sets of high-affinity IgE receptor (FcepsilonR1) polymorphisms with aspirin-intolerant asthma

Abstract: The FCER1G-237A>G and FCERIA-344C>T polymorphisms may contribute to the development of AIA in a Korean population.

Cited by 43 publications

References 29 publications

Genetic variability of the high-affinity IgE receptor α-subunit (FcεRIα)

Genetic variability of the high-affinity IgE receptor α-subunit (FcεRIα)

Genetic Variants of Thymic Stromal Lymphopoietin in Nonsteroidal Anti-Inflammatory Drug-Induced Urticaria/Angioedema

Adverse Immunological Reactions to Drugs

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