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1.
Gyu-Young Hur Young-Min Ye Dong-Hee Koh Seung-Hyun Kim Hae-Sim Park 《Allergy, asthma & immunology research》2013,5(6):371-376
Purpose
The IL-4 and IL-4 receptor α (IL-4Rα) genes are the key candidate genes for atopy and asthma susceptibility. Exposure to wheat flour can cause IgE sensitization and respiratory symptoms in bakery workers. Therefore, we hypothesized that IL-4 and IL-4Rα single nucleotide polymorphisms (SNPs) may be involved in the pathogenic mechanism of baker''s asthma.Methods
Clinical and genetic data from 373 bakery workers were analyzed. A survey questionnaire, spirometry, and skin prick tests with wheat flour were performed. Serum-specific IgE, IgG1, and IgG4 to wheat flour were determined using ELISA. Five candidate IL-4 (-729 T>G, 589 T>C, and 33 T>C) and IL-4Rα (Ile75Val A>G and Gln576Arg A>G) SNPs were genotyped and analyzed.Results
Workers with the G allele of IL-4Rα Ile75Val A>G had a significantly higher prevalence of work-related lower respiratory symptoms than those with the AA genotype (P=0.004, 16.0% vs. 2.9%). In the skin prick test, workers with the AA genotype of IL-4Rα Gln576Arg A>G had a significantly higher positive rate to wheat flour (P=0.015, 8.2% vs. 1.1%) than those with AG/GG genotype. No significant associations were found in the three genetic polymorphisms of IL-4. For the predicted probabilities, workers with the AA genotype of Gln576Arg A>G had a higher prevalence of IgG1 and IgG4 in response to wheat flour, according to increased exposure intensity (P=0.001 for IgG1 and P=0.003 for IgG4).Conclusions
These findings suggest that the IL-4Rα Ile75Val and Gln576Arg polymorphisms may be associated with work-related respiratory symptom development. 相似文献2.
Sae‐H Kim J‐E Lee Sang‐H Kim Y‐K Jee Y‐K Kim H‐S Park K‐U Min H‐W Park The Adverse Drug Reaction Research Group in Korea 《Clinical and experimental allergy》2009,39(12):1852-1856
Background The danger hypothesis provides a new perspective of the mechanisms underlying drug allergy. In this study, we evaluated associations between variations in the genes involved in danger signal pathways and antibiotic‐induced cutaneous allergic reactions (AICARs). Methods Two hundred cases with urticaria, angio‐oedema, maculopapular rash, and erythema multiforme caused by antibiotics were extracted from the database of the Adverse Drug Reaction Research Group in Korea. All cases were confirmed by an allergy specialist. Causative antibiotics included penicillin, cephalosporin, quinolone, and others (approximately 40 different types). Ten single nucleotide polymorphisms (SNPs) in seven genes (?318C>T, +49A>G, and +6230G>A in CTLA4, IVS+17T>C in CD28, ?3479T>G and I170V in CD86, ?1C>T in CD40, ?3458A>G in CD40LG, ?308G>A in TNF, and ?31T>C in IL1B) were scored for cases and for healthy subjects without a history of AICARs. Results Our analysis failed to reveal differences in the distribution of the 10 SNPs between cases and controls. However, we could find a gene–gene interaction between ?1C>T in CD40 and ?3458A>G in CD40L using multifactor dimensionality reduction analysis. Subjects with minor alleles of both SNPs showed a significant risk for developing AICARs [P=0.017, odds ratio (OR) (95% confidence interval)=2.93 (1.20–7.97)]. Conclusion Our findings suggest that a genetic interaction between CD40 and CD40L favours the development of AICARs. 相似文献
3.
4.
Jian Gao 《Brazilian journal of medical and biological research》2013,46(3):311-317
The multidrug resistance 1 gene (MDR1) is an important candidate
gene for influencing susceptibility to hepatocellular carcinoma (HCC). The
objective of the present study was to evaluate the association of
MDR1 polymorphisms with the risk of HCC in the Chinese Han
population. A total of 353 HCC patients and 335 healthy subjects were enrolled
in the study. Polymerase chain reaction-restriction fragment length polymorphism
(PCR-RFLP), created restriction site-PCR (CRS-PCR) and DNA sequencing methods
were used to identify MDR1 gene polymorphisms. Two allelic
variants (c.335T>C and c.3073A>C) were detected. The CC genotype of the
c.335T>C polymorphism was associated with an increased risk of developing HCC
compared to the TT genotype (OR = 2.161, 95%CI = 1.350-3.459, χ2 =
10.55, P = 0.0011). The risk of HCC was significantly higher for the CC genotype
in the c.3073A>C polymorphism compared to the AA genotype in the studied
populations (CC vs AA: OR = 2.575, 95%CI = 1.646-4.028,
χ2 = 17.64, P < 0.0001). The C allele of the c.335T>C and
c.3073A>C variants may contribute to the risk of HCC (C vs T
of c.335T>C: OR = 1.512, 95%CI = 1.208-1.893, χ2 = 13.07, P =
0.0003, and C vs A of c.3073A>C: OR = 1.646, 95%CI =
1.322-2.049, χ2 = 20.03, P < 0.0001). The c.335T>C and
c.3073A>C polymorphisms of the MDR1 gene were associated
with the risk of occurrence of HCC in the Chinese Han population. Further
investigations are needed to confirm these results in larger different
populations. 相似文献
5.
Lee HS Kim SH Kim KW Baek JY Park HS Lee KE Hong JY Kim MN Heo WI Sohn MH Kim KE 《Allergy, asthma & immunology research》2012,4(1):31-36
Purpose
Histamine N-methyltransferase (HNMT) catalyzes one of two major histamine metabolic pathways. Histamine is a mediator of pruritus in atopic dermatitis (AD). The aim of this study was to evaluate the association between HNMT polymorphisms and AD in children.Methods
We genotyped 763 Korean children for allelic determinants at four polymorphic sites in the HNMT gene: -465T>C, -413C>T, 314C>T, and 939A>G. Genotyping was performed using a TaqMan fluorogenic 5'' nuclease assay. The functional effect of the 939A>G polymorphism was analyzed.Results
Of the 763 children, 520 had eczema and 542 had atopy. Distributions of the genotype and allele frequencies of the HNMT 314C>T polymorphism were significantly associated with non-atopic eczema (P=0.004), and those of HNMT 939A>G were significantly associated with eczema in the atopy groups (P=0.048). Frequency distributions of HNMT -465T>C and -413C>T were not associated with eczema. Subjects who were AA homozygous or AG heterozygous for 939A>G showed significantly higher immunoglobulin E levels than subjects who were GG homozygous (P=0.009). In U937 cells, the variant genotype reporter construct had significantly higher mRNA stability (P<0.001) and HNMT enzyme activity (P<0.001) than the common genotype.Conclusions
Polymorphisms in HNMT appear to confer susceptibility to AD in Korean children. 相似文献6.
Jolanta Wasilewska Maciej Kaczmarski Anna Stasiak-Barmuta Jolanta Tobolczyk Ewa Kowalewska 《Archives of Medical Science》2012,8(2):324-331
Introduction
Immune system dysfunction is considered to be one of many medical disorders found in children with autism. The primary objective of the study was to assess if blood tests reflecting humoral immunity (IgA, IgG, IgM, IgE) are useful in identifying children with regressive autism. The secondary objective was to evaluate a part of the cellular arm of immunity (CD4/CD25 Tregs, CD4/CD23 cells) in those children.Material and methods
Using a clinical case-control design, the systemic levels of immunoglobulins and lymphocyte subpopulations analysed by flow cytometry were compared in children aged 3-6 years old with a new diagnosis of regressive autism (n = 24; mean age: 4.25 ±1.70 years; male 23/24) and in sex- and age-matched healthy children (n = 24; aged 4.25 ±2.20 years; male 23/24).Results
The humoral immunity profile, described by three binary variables, IgA < 0.97 g/l, IgE > 36 IU/ml, and IgG > 6.3 g/l, with a sensitivity of 79% and a specificity of 83% (p < 0.0001), was able to identify children with autism. The highest risk of autism diagnosis was associated with IgA < 0.97g/l (OR – 23.0; p < 0.001). A higher number of CD19/CD23 was found in children diagnosed with autism than in the control group (36.82 ±6.72% vs. 18.20 ±3.95%; p < 0.02). No correlation between the number of CD23-positive cells and serum IgE levels was observed.Conclusions
A subtle shift of serum immunoglobulins consisting of low-normal IgA and B cell activation expressed by an increase of CD23-positive cells may characterize children with regressive autism aged 3-6 years old. 相似文献7.
《European journal of human genetics : EJHG》2016,24(1):66-72
Alkaptonuria (AKU) is an autosomal recessive disorder caused by mutations in homogentisate-1,2-dioxygenase (HGD) gene leading to the deficiency of HGD enzyme activity. The DevelopAKUre project is underway to test nitisinone as a specific treatment to counteract this derangement of the phenylalanine-tyrosine catabolic pathway. We analysed DNA of 40 AKU patients enrolled for SONIA1, the first study in DevelopAKUre, and of 59 other AKU patients sent to our laboratory for molecular diagnostics. We identified 12 novel DNA variants: one was identified in patients from Brazil (c.557T>A), Slovakia (c.500C>T) and France (c.440T>C), three in patients from India (c.469+6T>C, c.650–85A>G, c.158G>A), and six in patients from Italy (c.742A>G, c.614G>A, c.1057A>C, c.752G>A, c.119A>C, c.926G>T). Thus, the total number of potential AKU-causing variants found in 380 patients reported in the HGD mutation database is now 129. Using mCSM and DUET, computational approaches based on the protein 3D structure, the novel missense variants are predicted to affect the activity of the enzyme by three mechanisms: decrease of stability of individual protomers, disruption of protomer-protomer interactions or modification of residues in the region of the active site. We also present an overview of AKU in Italy, where so far about 60 AKU cases are known and DNA analysis has been reported for 34 of them. In this rather small group, 26 different HGD variants affecting function were described, indicating rather high heterogeneity. Twelve of these variants seem to be specific for Italy. 相似文献
8.
Francisco Javier León Fernando Rondón Clara Inés Vargas Myriam Oróstegui Leonelo Bautista Norma Cecilia Serrano María c Páez Adriana Castillo 《Colombia Médica》2012,43(2):154-161
Introduction:
In spite of nearly 40% of variability in blood pressure being explained by genetic factors, the identification of genes associated with essential high blood pressure is difficult to determine in populations where individuals have different genetic backgrounds. In these circumstances it is necessary to determinate whether the population is sub-structured because this can bias studies associated with this disease.Objective:
To determine the genetic structure of the population in Bucaramanga from genetic polymorphisms associated with the regulation of blood pressure: 448G>T, 679C>T y 1711C>T from the gene kinase 4 of the dopaminergic receptor linked to the protein G and Glu298Asp, -786T>C and the VNTR of the intron 4 of the gene of endothelial nitric oxide.Methods:
A sample of 552 unrelated individuals was studied through analysis of restriction fragment length polymorphism. The allelic, haplotypic and genotypic frequencies were calculated, the Hardy-Weinberg equilibrium was determined and a molecular analysis of variance was performed to determine the genetic structure.Results:
Thirty-eight (38) Haplotypes were identified with GCCTG4b being the most frequent (21.2%). The most diverse polymorphism was 448G>T with a frequency of 49.9% for heterozygous. The six polymorphisms were found in genetic equilibrium and a genetic structure of populations was not evidenced (FST= 0.0038).Conclusion:
The population studied does not present a genetic sub-structure and the polymorphisms analyzed were found in genetic equilibrium. This indicates that the population mixes randomly and there are no sub-groups capable of affecting the results of the association studies. 相似文献9.
Jun Wang Xufeng Guo Jixiang Zhang Jia Song Mengyao Ji Shijie Yu Jing Wang Zhuo Cao Weiguo Dong 《Yonsei medical journal》2013,54(6):1353-1361
Purpose
Four polymorphisms, -765G>C, -1195G>A, 8473T>C, and Val511Ala, in the cyclooxygenase-2 (COX-2) gene were identified to be associated with colorectal cancer (CRC) risk. However, the results are inconsistent. The objective of this meta-analysis was to evaluate the association between these four polymorphisms and the risk of CRC.Materials and Methods
All eligible case-control studies published up to December 2012 on the association between the four polymorphisms of COX-2 and CRC risk were identified by searching PubMed and Web of Science. The CRC risk associated with the four polymorphisms of the COX-2 gene was estimated for each study by odds ratio (OR) together with its 95 % confidence interval (CI), respectively.Results
A total of 15 case-control studies were included. Overall, no evidence has indicated that the -1195A allele, -765C allele, 8473C allele, and 511Ala allele are associated with susceptibility to CRC (-1195G>A: OR=1.11, 95 % CI: 0.82-1.51, p=0.78; -765G>C: OR=1.08, 95 % CI: 0.96-1.21, p=0.07; 8473T>C: OR=1.03, 95 % CI: 0.89-1.18, p=0.91; Val511Ala: OR=0.71, 95 % CI: 0.46-1.09, p=0.94). However, stratified analysis with ethnicity indicated that individuals with -765GC or GC/CC genotypes had an increased risk of CRC among Asian populations (GC vs. GG: OR=1.05, 95 % CI: 0.87-1.28, p=0.03; GC+CC vs. GG: OR=1.08, 95 % CI: 0.96-1.21, p=0.07).Conclusion
This meta-analysis indicated that -765G>C polymorphism was significantly associated with susceptibility to CRC in Asian populations. 相似文献10.
Altered CD45 expression in C77G carriers influences immune function and outcome of hepatitis C infection 总被引:3,自引:0,他引:3
Dawes R Hennig B Irving W Petrova S Boxall S Ward V Wallace D Macallan DC Thursz M Hill A Bodmer W Beverley PC Tchilian EZ 《Journal of medical genetics》2006,43(8):678-684
Background
A polymorphism in exon 4 (C77G) of CD45 that alters CD45 splicing has been associated with autoimmune and infectious diseases in humans.Objective
To investigate the effect of C77G in hepatitis C virus (HCV) infected individuals and study the phenotype and function of peripheral blood mononuclear cells (PBMC) from healthy and hepatitis C infected C77G carriers.Results
C77G individuals showed an increased proportion of primed CD45RA and effector memory CD8 T cells and more rapid activation of the lymphocyte specific protein tyrosine kinase (Lck) following CD3 stimulation. Transgenic mice with CD45 expression mimicking that in human C77G variants had more activated/memory T cells, more rapid proliferative responses, and activation of Lck.Conclusions
Changes in CD45 isoform expression can alter immune function in human C77G variants and CD45 transgenic mice. The C77G allele may influence the outcome of HCV infection. 相似文献11.
Tanja Lippmann Sandra M Pasternack Britta Kraczyk Sabine E Dudek Gabriele Dekomien 《Journal of negative results in biomedicine》2006,5(1):1-5
Background
Chronic inflammation is a risk factor for colorectal cancer and polymorphisms in the inflammatory genes could modulate the levels of inflammation. We have investigated ten single nucleotide polymorphisms (SNPs) in the following inflammation-related genes: TLR4 (Asp299Gly), CD14 (-260 T>C), MCP1 (-2518 A>G), IL12A (+7506 A>T, +8707 A>G, +9177 T>A, +9508 G>A), NOS2A (+524T>C), TNF (-857C>T), and PTGS1 (V444I) in 377 colorectal (CRC) cancer cases and 326 controls from Barcelona (Spain).Results
There was no statistically significant association between the SNPs investigated and colorectal cancer risk.Conclusion
The lack of association may show that the inflammatory genes selected for this study are not involved in the carcinogenic process of colorectum. Alternatively, the negative results may derive from no particular biological effect of the analysed polymorphisms in relation to CRC. Otherwise, the eventual biological effect is so little to go undetected, unless analysing a much larger sample size. 相似文献12.
Purevsuren Losol Seung-Hyun Kim Eui-Kyung Hwang Yoo Seob Shin Hae-Sim Park 《Allergy, asthma & immunology research》2013,5(2):106-109
Interleukin 5 (IL-5) is a key cytokine involved in the induction of T-helper type 2 (Th2) responses in the asthmatic airway. We investigated IL-5 genetic polymorphisms associated with asthma phenotypes, including IgE responses to staphylococcal enterotoxins A and B (SEA and SEB, respectively), in asthmatics. Adult asthmatics (n=310) and normal controls (n=160) were enrolled in the present study. Serum total and specific IgE to SEA and SEB were measured. Two IL-5 polymorphisms, -746A>G and +4499T>G, were genotyped using the primer-extension method. There were no significant differences in genotype or haplotype frequencies of these polymorphisms between the two groups. Asthmatics carrying the AG/GG genotype at -746A>G had a significantly higher prevalence of serum specific IgE to SEA (P=0.008), higher total IgE levels (P=0.014), and lower PC20 methacholine levels (P=0.002) compared to those with the AA genotype. These findings suggest that the IL-5 promoter polymorphism at -746A>G enhances serum total and specific IgE responses to SEA, which may augment airway hyperresponsiveness in adult asthmatics. 相似文献
13.
Xuedong Shen Wilbert S. Aronow Chandra K. Nair Hema Korlakunta Mark J. Holmberg Fenwei Wang Stephanie Maciejewski Dennis J. Esterbrooks 《Archives of Medical Science》2011,7(1):61-66
Introduction
We hypothesized a relationship between severity of thoracic aortic atheroma (AA) and prevalence of high-risk coronary anatomy (HRCA).Material and methods
We investigated AA diagnosed by transesophageal echocardiography and HRCA diagnosed by coronary angiography in 187 patients. HRCA was defined as ≥ 50% stenosis of the left main coronary artery or significant 3-vessel coronary artery disease (≥ 70% narrowing).Results
HRCA was present in 45 of 187 patients (24%). AA severity was grade I in 55 patients (29%), grade II in 71 patients (38%), grade III in 52 patients (28%), grade IV in 5 patients (3%), and grade V in 4 patients (2%). The area under receiver operating characteristic curve for AA grade predicting HRCA was 0.83 (p = 0.0001). The cut-off points of AA to predict HRCA was > II grade. The sensitivity and specificity of AA > grade II to predict HRCA were 76% and 81%, respectively. After adjustment for 10 variables with significant differences by univariate regression, AA > grade II was related to HRCA by multivariate regression (odds ratio = 7.5, p< 0.0001). During 41-month follow-up, 15 of 61 patients (25%) with AA >grade II and 10 of 126 patients (8%) with AA grade ≤ 2 died (p= 0.004). Survival by Kaplan-Meier plot in patients with AA > grade II was significantly decreased compared to patients with AA ≤ grade II (p= 0.002).Conclusions
AA > grade II is associated with a 7.5 times increase in HRCA and with a significant reduction in all-cause mortality. 相似文献14.
Nami Shrestha Palikhe Seung-Hyun Kim Bo-Young Cho Gil-Soon Choi Joo-Hee Kim Young-Min Ye Hae-Sim Park 《Allergy, asthma & immunology research》2010,2(2):134-140
Purpose
Aspirin-intolerant asthma (AIA) is characterized by moderate to severe asthma that is aggravated by aspirin or other non-steroidal anti-inflammatory drugs. Affected patients frequently have chronic rhinosinusitis and nasal polyposis due to persistent upper and lower airway inflammation with marked eosinophilia. IL-13 plays a crucial role in the development of allergic asthma by inducing airway eosinophilia and hyper-reactivity and it has been correlated with an increased eosinophil count.Methods
Two promoter polymorphisms of the IL-13 gene (-1510 A>C and -1055C>T) and one coding nonsynonymus Arg110Gln (110G>A) polymorphism were genotyped using primer extension methods in 162 patients with AIA, 301 patients with aspirin-tolerant asthma (ATA), and 430 normal healthy controls (NC).Results
There was no significant difference in the genotype, allele, and haplotype frequencies of the three polymorphisms among the three groups. AIA patients with the AA genotype -1510A>C (P=0.012) and CC genotype -1055C>T (P<0.001) had a significantly higher frequency of rhinosinusitis, as compared to those with the minor alleles of these two single nucleotide polymorphisms. AIA patients with the GG genotype had a higher peripheral eosinophil count (P=0.025) and a higher serum eotaxin-1 level (P=0.044), as compared to patients with the AA genotype IL-13 Arg110Gln (110G>A).Conclusions
These findings suggest that the IL-13 polymorphisms at -1510A>C and 1055C>T are associated with the development of rhinosinusitis in AIA patients. IL-13 Arg110Gln may be associated with an increased eosinophil count and eotaxin-1 level and could increase eosinophilic inflammation in the upper and lower airways of patients with AIA. 相似文献15.
Purpose
To distinguish lupus flare-up from infection in systemic lupus erythematosus (SLE), we analyze the expression of circulating CD27high plasma cells in SLE patients with and without infection, in comparison to non-SLE patients with infection.Materials and Methods
The percentage of circulating CD27high plasma cells was measured by flow cytometry in the following four groups: 36 SLE patients without infection, 23 SLE patients with infection, eight non-SLE patients with infection, and 26 healthy controls.Results
The frequency of CD27high plasma cells had a correlation with the SLE disease activity index (SLEDAI) (r = 0.866, p < 0.05), level of anti-dsDNA (r = 0.886, p < 0.05), C3 (r = - 0.392, p < 0.05), and C4 (r = - 0.337, p < 0.05) in SLE patients without infection, but there was no correlation with disease activity in SLE patients with infection. Among three groups in particular-SLE without infection, SLE with infection, and non-SLE with infection-the percentages of CD27high plasma cells were elevated. The percentage of CD27high plasma cells was higher in SLE patients with infection, when compared to SLE patients without infection.Conclusion
The percentage of CD27high plasma cells is a biomarker for disease activity of SLE without infection, under correlation with SLEDAI, anti-dsDNA, and C3 and C4 level. However, when the SLE patients have an infection, the percentage of CD27high plasma cells is not an adequate biomarker for the survey of disease activity. The percentage of CD27high plasma cells may serve as a potential parameter to distinguish a lupus flare-up from infection. 相似文献16.
Ruizhong Zhang Yan Zou Jinhong Zhu Xinhao Zeng Tianyou Yang Fenghua Wang Jing He Huimin Xia 《International journal of medical sciences》2016,13(2):133-138
A previous genome-wide association study (GWAS) has found that some common variations in the BARD1 gene were associated with neuroblastoma susceptibility especially for high-risk subjects, and the associations have been validated in Caucasians and African-Americans. However, the associations between BARD1 gene polymorphisms and neuroblastoma susceptibility have not been studied among Asians, not to mention Chinese subjects. In the present study, we investigated the association of three BARD1 polymorphisms (rs7585356 G>A, rs6435862 T>G and rs3768716 A>G) with neuroblastoma susceptibility in 201 neuroblastoma patients and 531 controls using TaqMan methodology. Overall, none of these polymorphisms was significantly associated with neuroblastoma susceptibility. However, stratified analysis showed a more profound association between neuroblastoma risk and rs6435862 TG/GG variant genotypes among older children (adjusted OR=1.55, 95% CI=1.04-2.31), and children with adrenal gland-originated disease (adjusted OR=2.94, 95% CI=1.40-6.18), or with ISSN clinical stages III+IV disease (adjusted OR=1.75, 95% CI=1.09-2.84). Similar results were observed for the variant genotypes of rs3768716 A>G polymorphism among these three subgroups. Our results suggest that the BARD1 rs6435862 T>G and rs3768716 A>G polymorphisms may contribute to increased susceptibility to neuroblastoma, especially for the subjects at age ≥12 months, with adrenal gland-originated or with late clinical stage neuroblastoma. These findings need further validation by prospective studies with larger sample size with subjects enrolled from multicenter, involving different ethnicities. 相似文献
17.
Sailesh Palikhe Seung-Hyun Kim Le Duy Pham Young-Min Ye Hae-Sim Park 《Allergy, asthma & immunology research》2015,7(3):290-294
Protein tyrosine phosphatase-22 (PTPN22) gene encodes lymphoid-specific tyrosine phosphatase (Lyp), an inhibitor of T cell activation. A polymorphism of the PTPN22 gene has been found to be associated with chronic urticaria (CU). We investigated the associations between PTPN22 gene polymorphisms and CU characteristics, including serum specific IgE antibodies response to toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin A (SEA). CU patients (n=409) and normal healthy controls (n=388) were enrolled in the present study. Serum specific IgE to TSST-1 and SEA were measured by ImmunoCAP®. Five PTPN22 single nucleotide polymorphisms, -1123G>C, 1858C>T, 13145A>G, 14943C>T, and 20628A>G, were genotyped. There were no significant differences in genotype or haplotype frequencies of these polymorphisms between the 2 groups. CU patients carrying the GG genotype at 20628A>G (P=0.035) or haplotype 3 [GGG] (P=0.047) had a significantly higher prevalence of serum specific IgE to TSST-1 compared to non-carriers. Similarly, CT/TT genotype at 14943C>T had a significantly higher prevalence of serum specific IgE to SEA (P=0.045). The findings suggest that the PTPN22 gene polymorphisms at 20628A>G and 14943C>T may enhance serum specific IgE responses to TSST-1 and SEA, which may contribute to CU pathogenesis. 相似文献
18.
OBJECTIVES:
Atherosclerosis is a chronic inflammatory disease. Research has focused on identifying specific serum biomarkers to detect vulnerable plaques. These markers serve as diagnostic tools for acute coronary syndrome and assist in identifying high-risk patients. However, the existing data are limited and conflicting. This study tested the hypothesis that CD137 levels identify patients with acute coronary syndrome who are at a heightened risk for recurrent cardiac events.METHODS:
The levels of soluble CD137 (sCD137) were measured using ELISA in 180 patients with acute coronary syndrome and 120 patients with acute chest pain. Platelet activation was assessed by flow cytometry. Receiver operating characteristic curve analysis was performed to evaluate the prognostic characteristics of sCD137.RESULTS:
The levels of sCD137 were elevated in 75 patients with acute coronary syndromes and 20 patients with acute chest pain (>35.0 ng/ml). In patients with acute coronary syndrome, elevated sCD137 levels (>35.0 ng/ml) indicated an increased risk for major adverse cardiovascular events (OR = 1.93, 95% CI: 1.39-2.54). Elevated serum levels of sCD137 and cTnT were correlated with a significantly increased risk of major adverse cardiovascular events in both groups after 30 days, six months and nine months of follow-up. The increased sCD137 levels were significantly correlated with the levels of troponin I (r = 0.4799, p<0.001). Importantly, 26 patients with normal cTnI levels had acute coronary syndrome. However, elevated sCD137 levels identified these patients as a being high-risk subgroup (OR = 2.14, 95% CI: 1.25-4.13).CONCLUSIONS:
Elevated sCD137 levels indicate an increased risk of cardiovascular events in patients with acute coronary syndrome. Soluble CD137 may be a useful prognostic marker or indicator for adverse events in patients with acute coronary syndrome. 相似文献19.
Expression of CD5 and CD72 on T and B cell subsets in rheumatoid arthritis and Sjögren's syndrome. 下载免费PDF全文
C Jamin A Lamour Y L Pennec M Hirn P Le Goff P Youinou 《Clinical and experimental immunology》1993,92(2):245-250
A minority of B cells express the CD5 marker, which is found on virtually all T cells, and CD72 has been defined as the CD5 ligand on the B cell membrane. The mean fluorescence intensity (MFI) of the CD5 molecules was shown to be higher on CD4+CD29+ than CD4+CD45RA+ in peripheral blood (PB) and synovial fluid (SF) of rheumatoid arthritis (RA) patients (P < 0.0001 and < 0.001), and PB of Sjögren's syndrome (SS) patients and normal controls (P < 0.02 and < 0.03). This MFI declined once the CD4 expressed HLA-DR in PB of SS patients (P < 0.004) and normal controls (P < 0.02) or CD25 in PB of RA (P < 0.004) and SS patients (P < 0.0004). There was a correlation between the CD5 MFI on CD4+CD45RA+ and CD4+CD29+ in RA (P < 0.001) as well as SS (P < 0.0007) PB. The CD72 MFI was impressively higher on CD5+ than CD5- B cells in PB and SF of RA patients (P < 0.0001 and P < 0.005) and PB of SS patients (P < 0.005) and normal controls (P < 0.005). Our data suggest that, in association with CD4CD29, CD5 is involved in CD5+B/CD5+ B cell interactions in non-organ-specific autoimmune diseases. 相似文献
20.
Angela M Monteiro da Silva Francisco A B Speranza Solange Kiyoko Ishii Raphael Hirata Jr Ana Luíza Mattos-Guaraldi Lucimar Gon?alves Milagres 《Clinics (S?o Paulo, Brazil)》2015,70(2):152-156