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Query Topic: TNFSF15

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tumor necrosis factor ligand(5)

Association study between two polymorphisms of tumor necrosis factor ligand superfamily member 15 (TNFSF15) gene and ulcerative colitis in south-west of Iran.
BACKGROUND AND AIMS: Ulcerative colitis (UC) is the most prevalent clinical manifestation of the inflammatory bowel disease (IBD). Several candidate genes have been suggested to be involved in the genetic susceptibility or resistance in the development of UC. Among them, tumor necrosis factor ligand superfamily member 15 (TNFSF15) have been reported in association with IBD in several studies. The aim of this study was to investigate the association of TNFSF15 gene polymorphisms located in the promoter region, including rs6478108 (G/A -9706) and rs3810936 (G/A -15524) in Iranian patients with UC. METHODS: In this way, the two single nucleotide polymorphisms were studied in 115 patients with UC and 115 healthy controls with the same ethnic group from south-west of Iran. The genomic DNA of samples was genotyped using TaqMan Real-time PCR assay. This case-control study was conducted at the Department of Immunology, Jundishapur University of Medical Sciences, Ahvaz, Iran. RESULTS AND CONCLUSION: Our results did not confirm the formerly reported association of the studied polymorphisms with UC disease in comparison with healthy controls, neither with the type of the clinical forms of Colitis in the studied Iranian population. Comparing the genotype frequency of single nucleotide polymorphism (SNP) rs6478108, wild-type homozygous and heterozygote and mutant homozygote were 33%, 55.7%, and 11.3% in cases vs. 34.8%, 50.4%, and 14.8% in the controls (P = 0.6). The genotype frequency of SNP rs3810936 were 20.9%, 40.9%, and 38.2% in the cases compared to 18.3%, 44.3%, and 37.4% in controls, which was not significant ( P = 0.8). As multiple ethnic groups reside in all around the country, further studies using different ethnicities and/or larger sample size are required to clarify the role of these polymorphisms in the genetic susceptibility of UC in Iranian populations.
Publication Date: 2018-12-18
Journal: Journal of cellular biochemistry


vascular endothelial cells(6)

VEGI Improves Outcomes in the Early Phase of Experimental Traumatic Brain Injury.
Excessive expression of vascular endothelial growth factor (VEGF) is a common cause of blood-brain barrier (BBB) breakdown that triggers severe complications following traumatic brain injury (TBI). It has been shown that inhibition of VEGF activities may attenuate cerebral edema in pathological conditions. Vascular endothelial growth inhibitor (VEGI; also known as TNFSF15), a cytokine produced largely by vascular endothelial cells, is capable of downregulating VEGF expression and inhibiting VEGF receptor-2 (VEGFR2) activation. In this study we found that TBI can cause breakdown of BBB and sharp increases of VEGF/VEGI and Angpt2/Angpt1 ratios in the injured tissues. VEGI treatment resulted in a marked decrease of BBB permeability and concomitant restoration of normal ratios of VEGF/VEGI and Angpt2/Angpt1. Consistently, alleviated edema, decreased neuron cell death, and improved neurological functions were observed when the experimental animals were treated with VEGI in the early phase of TBI. Our findings suggest that administration of VEGI recombinant protein at early phases of TBI is beneficial to stabilization of the disease conditions.
Publication Date: 2020-05-08
Journal: Neuroscience


tnfsf15 snps(6)

Association of Genetic Variations in TNFSF15 With Acute Anterior Uveitis in Chinese Han.
T cells play an important role in the pathogenesis of uveitis. Recent studies have indicated that the TNFSF15 gene that encodes the TL1A protein can regulate the differentiation and activation of T cells. TNFSF15 gene polymorphisms have been found to be associated with several autoimmune disorders. A possible association of TNFSF15 with acute anterior uveitis (AAU) has not yet been reported and was therefore the purpose of our study. Eight single nucleotide polymorphisms (SNPs) were examined using TaqMan SNP Genotyping Assay or PCR-restriction fragment length polymorphism in 983 AAU patients and 1128 healthy controls. Genotype distributions and allele frequencies were compared using χ2 analysis between AAU patients and healthy controls. Stratified analysis was also performed according to ankylosing spondylitis (AS) status. The TNFSF15 mRNA expression was quantified by real-time PCR. A significantly decreased frequency of the TT genotype in TNFSF15-rs3810936 was found in AAU patients (P = 6.36 × 10(-6), corrected P[Pc] = 1.52 × 10(-4), OR = 0.6, 95% CI = 0.5-0.8). Stratification according to AS status did not reveal a difference concerning the association with TNFSF15-rs3810936. None of the other TNFSF15 SNPs tested were associated with AAU. This study shows an association between TNFSF15-rs3810936 and AAU and suggests that the TL1A/DR3 pathway may be implicated in the pathogenesis of this disease.
Publication Date: 2015-07-23
Journal: Investigative ophthalmology & visual science


tnfsf15 vegi(5)

Vascular endothelial growth factor suppresses TNFSF15 production in endothelial cells by stimulating miR-31 and miR-20a expression via activation of Akt and Erk signals.
Tumor necrosis factor superfamily-15 (TNFSF15; VEGI; TL1A) is a negative modulator of angiogenesis for blood vessel homeostasis and is produced by endothelial cells in a mature vasculature. It is known to be downregulated by vascular endothelial growth factor (VEGF), a major regulator of neovascularization but the mechanism of this interaction is unclear. Here we report that VEGF is able to stimulate the production of two microRNAs, miR-20a and miR-31, which directly target the 3'-UTR of TNFSF15. Additionally, we show that two VEGF-stimulated cell growth signals, Erk and Akt, are responsible for promoting the expression of miR-20a and miR-31. Treatment of human umbilical vein endothelial cells (HUVECs) with Akt inhibitor LY294002 results in diminished miR-20a and miR-31 production, while Erk inhibitor U0126 prevented VEGF-stimulated expression of miR-20a but not that of miR-31. Furthermore, inactivation of either Erk or Akt signals restores TNFSF15 gene expression. In an angiogenesis assay, elevated miR-20a or miR-31 levels in HUVECs leads to enhancement of capillary-like tubule formation
Publication Date: 2017-01-18
Journal: FEBS open bio


rs6478108 rs6478109(5)

Diverticulitis and Crohn's disease have distinct but overlapping tumor necrosis superfamily 15 haplotypes.
Diverticulitis (DD) and Crohn's disease (CD) have overlapping features including bowel structuring, inflammation, and infection. Tumor necrosis superfamily 15 (TNFSF15) is an immunoregulatory, anti-angiogenic gene. CD has been previously associated with a haplotype of five TNFSF15 single-nucleotide polymorphism alleles: rs3810936 (G allele), rs6478108 (A), rs6478109 (G), rs7848647 (G), and rs7869487 (A). We aimed to determine the TNFSF15 risk haplotype for DD versus controls with a subgroup analysis of youthful DD patients (aged ≤55 y) versus older controls (aged ≥55 y). A total of 148 diverticulitis patients (90 aged ≤55 y) and 200 controls (87 aged ≥55 y) were genotyped using our custom-designed Illumina Veracode microarray chip. Genotypes from rs3810936, rs6478108, rs6478109, rs7848647, rs7869487 and two additional TNFSF15 single nucleotide polymorphisms, rs3810936 and rs11554257, were analyzed. PHASE version 2.1, R with HaploStats and the Broad Institute's Haploview program were used for statistics and imputed haplotype frequency. Permutation corrected for multiple comparisons. The CD GAGGA haplotype was significantly associated with diverticulitis (P = 0.03) in the all DD versus all controls comparison. A second haplotype, rs6478108 (A), rs6478109 (G), rs7869487 (A), and rs4263839 (G), was also associated with DD in this cohort (P = 0.025). A third haplotype rs6478108 (A), rs6478109 (G), rs7848647 (G) and rs7869487 (A), rs4263839 (G) was demonstrated in the DD < 55 versus controls >55 comparison (P = 0.045). Distinct but overlapping TNFSF15 haplotypes were demonstrated in diverticulitis patients versus healthy controls when compared with the known Crohn's risk haplotype suggesting similar but distinct genetic predispositions. This study strengthens the role for a genetic predisposition to diverticulitis that involves the TNFSF15 gene.
Publication Date: 2017-06-19
Journal: The Journal of surgical research


rs6478109 rs7848647(5)

Genetic analysis of TNFST15 variants in ankylosing spondylitis.
The purpose of this study was to explore the role of TNF-like ligand 1A (TL1A) gene (TNFST15) polymorphisms (rs3810936, rs7848647, and rs6478109) in the generation of ankylosing spondylitis (AS). Polymerase chain reaction (PCR) and sequencing were used to conduct the genotyping of TNFSF15 polymorphisms in 113 AS patients and 120 healthy persons as the case and control groups. The frequencies comparison was performed by chi-square or t test between the two groups. Odds ratio (OR) and 95% confidence interval (95% CI) were calculated to represent the correlation between TNFSF15 polymorphism and AS. Besides, genotypes distribution of the former in controls was checked by Hardy-Weinberg equilibrium (HWE). There was statistically significant difference in AS patients and controls based on family history. Among TNFSF15 polymorphisms, only TT genotype frequency of rs3810936 in cases was obviously high, compared with the controls (P=0.04), the results indicated that TT was a high-risk genotype (OR=2.31, 95% CI=1.03-5.20). However, both of rs6478109, rs7848647 polymorphisms didn't show any association with AS. Rs3810936 of TNFSF15 were related to the risk of AS and we should pay more attention to the role of TNFSF15 polymorphisms in the pathogenesis of AS in the future.
Publication Date: 2016-01-30
Journal: International journal of clinical and experimental pathology


disease ibd(5)

TNFSF15 Promotes Antimicrobial Pathways in Human Macrophages and These Are Modulated by TNFSF15 Disease-Risk Variants.
TNFSF15 genetic variants leading to increased TNF superfamily member 15 (TNFSF15) expression confer risk for inflammatory bowel disease (IBD), and TNFSF15 is being explored as a therapeutic target in IBD patients. Although the focus for TNFSF15-mediated inflammatory outcomes has been predominantly on its action on T cells, TNFSF15 also promotes inflammatory outcomes in human macrophages. Given the critical role for macrophages in bacterial clearance, we hypothesized that TNFSF15 promotes antimicrobial pathways in human macrophages and that macrophages from TNFSF15 IBD risk carriers with higher TNFSF15 expression have an advantage in these antimicrobial outcomes. We analyzed protein expression, signaling, bacterial uptake, and intracellular bacterial clearance in human monocyte-derived macrophages through flow cytometry, enzyme-linked immunosorbent assay, and gentamicin protection. Autocrine/paracrine TNFSF15 interactions with death receptor 3 (DR3) were required for optimal levels of pattern-recognition-receptor (PRR)-induced bacterial clearance in human macrophages. TNFSF15 induced pyruvate dehydrogenase kinase 1-dependent bacterial uptake and promoted intracellular bacterial clearance through reactive oxygen species, nitric oxide synthase 2, and autophagy up-regulation. The TNFSF15-initiated TNF receptor-associated factor 2/receptor-interacting protein kinase 1/RIP3 pathway was required for mitogen-activated protein kinase and nuclear factor-κB activation, and, in turn, induction of each of the antimicrobial pathways; the TNFSF15-initiated Fas-associated protein with death domain/mucosa-associated lymphoid tissue lymphoma translocation protein 1/caspase-8 pathway played a less prominent role in antimicrobial functions, despite its key role in TNFSF15-induced cytokine secretion. Complementation of signaling pathways or antimicrobial pathways restored bacterial uptake and clearance in PRR-stimulated macrophages where TNFSF15:DR3 interactions were inhibited. Monocyte-derived macrophages from high TNFSF15-expressing rs6478108 TT IBD risk carriers in the TNFSF15 region showed increased levels of the identified antimicrobial pathways. We identify that autocrine/paracrine TNFSF15 is required for optimal PRR-enhanced antimicrobial pathways in macrophages, define mechanisms regulating TNFSF15-dependent bacterial clearance, and determine how the TNFSF15 IBD risk genotype modulates these outcomes.
Publication Date: 2020-08-23
Journal: Cellular and molecular gastroenterology and hepatology


factor tnf(5)

Tumor Necrosis Factor-like Cytokine TL1A and Its Receptors DR3 and DcR3: Important New Factors in Mucosal Homeostasis and Inflammation.
Tumor necrosis factor (TNF)-like cytokine 1A (TL1A) is a member of the TNF superfamily of proteins (TNFSF15), which signals through association with death domain receptor 3 (DR3). Decoy receptor 3 (DcR3) competes with DR3 for TL1A binding and inhibits functional signaling. These proteins are significantly upregulated in inflamed intestinal tissues, and their pathogenetic importance for inflammatory bowel disease (IBD) is suggested by accumulating evidence. TL1A/DR3 induce costimulatory signals to activated lymphocytes, including the gut-specific populations of CD4+CD161+ and CD4+CCR9+ cells, affecting all major effector pathways and inducing the mucosal upregulation of Th1, Th2, and Th17 factors. They may also participate in mucosal homeostasis and defense against pathogens through their effects on the development and function of the recently described innate lymphoid cells. T-regulatory lymphocytes highly express DR3, and they respond to TL1A stimulation also. Mechanistic studies by transgenic expression of TL1A, deletion of TL1A or DR3, and therapeutic blockade by anti-TL1A antibodies all support the critical involvement of the corresponding pathways in the pathogenesis of chronic mucosal inflammation. Wide genome association studies have identified IBD-specific polymorphisms in TNFSF15 gene, which have functional implications and serve as poor prognostic factors. Recently, TL1A blockade in mice was presented as a unique pharmacological treatment for the reversal of established intestinal fibrosis. Finally, TL1A/DR3 signaling seems to critically participate in extraintestinal inflammatory conditions that are frequently associated with IBD as part of the gut-joint-skin-eye axis. These converging lines of evidence make TL1A/DR3 a suitable model for personalized approaches to IBD therapy.
Publication Date: 2015-06-23
Journal: Inflammatory bowel diseases


odds ratio(5)

Common risk variants in NPHS1 and TNFSF15 are associated with childhood steroid-sensitive nephrotic syndrome.
To understand the genetics of steroid-sensitive nephrotic syndrome (SSNS), we conducted a genome-wide association study in 987 childhood SSNS patients and 3,206 healthy controls with Japanese ancestry. Beyond known associations in the HLA-DR/DQ region, common variants in NPHS1-KIRREL2 (rs56117924, P=4.94E-20, odds ratio (OR) =1.90) and TNFSF15 (rs6478109, P=2.54E-8, OR=0.72) regions achieved genome-wide significance and were replicated in Korean, South Asian and African populations. Trans-ethnic meta-analyses including Japanese, Korean, South Asian, African, European, Hispanic and Maghrebian populations confirmed the significant associations of variants in NPHS1-KIRREL2 (P
Publication Date: 2020-06-20
Journal: Kidney international


cirrhosis pbc(4)

Disease susceptibility genes shared by primary biliary cirrhosis and Crohn's disease in the Japanese population.
We previously identified TNFSF15 as the most significant susceptibility gene at non-HLA loci for both primary biliary cirrhosis (PBC) and Crohn's diseases (CD) in the Japanese population. The aim of this study is to identify further disease susceptibility genes shared by PBC and CD. We selected 15 and 33 genetic variants that were significantly associated with PBC and CD, respectively, based on previously reported genome-wide association studies of the Japanese population. Next, an association study was independently performed for these genetic variants in CD (1312 CD patients and 3331 healthy controls) and PBC (1279 PBC patients and 1015 healthy controls) cohorts. Two CD susceptibility genes, ICOSLG rs2838519 and IL12B rs6556412, were also nominally associated with susceptibility to PBC (P=3.85 × 10(-2) and P=8.40 × 10(-3), respectively). Three PBC susceptibility genes, CXCR5 rs6421571, STAT4 rs7574865 and NFKB1 rs230534, were nominally associated with susceptibility to CD (P=2.82 × 10(-2), P=3.88 × 10(-2) and P=2.04 × 10(-2), respectively). The effect of ICOSLG and CXCR5 variants were concordant but the effect of STAT4, NFKB1 and IL12B variants were discordant for PBC and CD. TNFSF15 and ICOSLG-CXCR5 might constitute a shared pathogenic pathway in the development of PBC and CD in the Japanese population, whereas IL12B-STAT4-NFKB1 might constitute an opposite pathogenic pathway, reflecting the different balance between Th1 and Th17 in the two diseases.
Publication Date: 2015-06-19
Journal: Journal of human genetics


colitis uc(4)

Protective association of tumor necrosis factor superfamily 15 (TNFSF15) polymorphic haplotype with Ulcerative Colitis and Crohn's disease in an Indian population.
Tumor necrosis factor superfamily (TNFSF) proteins are involved in the genesis of inflammatory bowel disease (IBD). We examined the association of seven single nucleotide polymorphisms (SNP) in the TNFSF15 gene with Crohn's disease (CD) and ulcerative colitis (UC) in the Indian population. Seven SNPs in the TNFSF15 gene (rs10114470, rs3810936, rs6478108, rs4263839, rs6478109, rs7848647 and rs7869487) were genotyped in 309 CD patients, 330 UC patients and 437 healthy controls using the Sequenom iPLEX MassArray platform. Disease associations were evaluated for allelotypes and for genotypes. The minor T alleles and the TT genotypes of rs10114470 and rs3810936 were significantly protectively associated with both CD and UC. The CC genotype of rs6478108, AA genotype of rs4263839, the AA genotype of rs6478109, the TT genotype of rs7848647 and the CC genotype of rs7869487 were all protectively associated with CD but not with UC. Two haplotype blocks could be discerned, one where SNPs rs10114470 and rs3810936 were in tight LD (D' = 0.8) and the other where rs6478108, rs4263839, rs6478109, rs7848647 and rs7869487 were in tight LD (D' 0.92-1.00). The second block of haplotypes were not associated with CD or with UC. The first block of haplotypes was very significantly associated with both CD and UC. Strong associations exist between TNFSF15 gene polymorphisms and IBD (both CD and UC) in the Indian population.
Publication Date: 2014-12-17
Journal: PloS one


tl1a tnfsf15(4)

DcR3 promotes hepatoma cell migration by downregulating E-cadherin expression.
Decoy receptor 3 (DcR3), a decoy molecule belonging to the tumor necrosis factor receptor superfamily (TNFRSF), is a soluble receptor that can neutralize the biological effects of three other TNFSF members, namely, Fas ligand (FasL/TNFSF6/CD95L), LIGHT (TNFSF14) and TNF-like molecule 1A (TL1A/TNFSF15). DcR3 expression is increased in tumor cells. As such, DcR3 has been considered a potential biomarker to predict cancer invasion and progression of inflammation. However, the molecular mechanisms of DcR3 in tumor progression and metastasis remain poorly described. In the present study, DcR3 induced cytoskeleton remodeling, inhibited E-cadherin expression, and promoted cancer cell migration. Immunofluorescence and flow cytometry demonstrated that DcR3 expression was increased in hepatoma cells, whereas E-cadherin expression was significantly downregulated. Immunohistochemistry revealed that DcR3 and E-cadherin exhibited an opposite expression pattern between normal and cancerous liver tissues. Moreover, DcR3 treatment promoted IκBα degradation and p65 nuclear translocation. Therefore, the present study uncovered the mechanism underlying the function of DcR3 in cancer cell migration and provides evidence that DcR3 may be a potential target for cancer therapy.
Publication Date: 2017-06-01
Journal: Oncology reports


c13orf31 nod2(3)

Genetic factors conferring an increased susceptibility to develop Crohn's disease also influence disease phenotype: results from the IBDchip European Project.
Through genome-wide association scans and meta-analyses thereof, over 70 genetic loci (Crohn's disease (CD) single nucleotide polymorphisms (SNPs)) are significantly associated with CD. We aimed to investigate the influence of CD-SNPs and basic patient characteristics on CD clinical course, and develop statistical models to predict CD clinical course. This retrospective study included 1528 patients with CD with more than 10 years of follow-up from eight European referral hospitals. CD outcomes of interest were ileal (L1), colonic (L2) and ileocolonic disease location (L3); stenosing (B2) or penetrating behaviour (B3); perianal disease; extraintestinal manifestations; and bowel resection. A complicated disease course was defined as stenosing or penetrating behaviour, perianal disease and/or bowel resection. Association between CD-SNPs or patient characteristics and specified outcomes was studied. Several CD-SNPs and clinical characteristics were statistically associated with outcomes of interest. The NOD2 gene was the most important genetic factor, being an independent predictive factor for ileal location (p=2.02 × 10(-06), OR=1.90), stenosing (p=3.16 × 10(-06), OR=1.82) and penetrating (p=1.26 × 10(-02), OR=1.25) CD behaviours, and need for surgery (p=2.28 × e-05, OR=1.73), and as such was also the strongest factor associated with a complicated disease course (p=6.86 × 10(-06), OR=2.96). Immunomodulator (azathioprine/6-mercaptopurine and methotrexate) use within 3 years after diagnosis led to a reduction in bowel stenoses (p=1.48 × 10(-06), OR=0.35) and surgical rate (p=1.71 × 10(-07), OR=0.34). Association between each outcome and genetic scores, created using significant SNPs in the univariate analysis, revealed large differences in the probability of developing fistulising disease (IL23R, LOC441108, PRDM1, NOD2; p=9.64e-4, HR=1.43), need for surgery (IRGM, TNFSF15, C13ORF31, NOD2; p=7.12 × 10(-03), HR=1.35), and stenosing disease (NOD2, JAK2, ATG16L1; p=3.01 × 10(-02), HR=1.29) among patients with low and high score. This large multicentre cohort study has found several genetic and clinical factors influencing the clinical course of CD. NOD2 and early immunomodulator use are the clinically most meaningful predictors for its clinical course.
Publication Date: 2012-12-25
Journal: Gut


tnfsf15 expression(3)

Erratum: Sustained TL1A (TNFSF15) expression on both lymphoid and myeloid cells leads to mild spontaneous intestinal inflammation and fibrosis (DOI: 10.1556/EuJMI.3.2013.1.2).
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Publication Date: 2013-11-23
Journal: European journal of microbiology & immunology


ligand superfamily(3)

HLA-C*01 is a Risk Factor for Crohn's Disease.
A dysregulated mucosal immune response to the intestinal environment in a genetically susceptible host is hypothesized to be critical to the pathogenesis of Crohn's disease (CD). Therefore, we examined CD-susceptibility genes involved in the immune response through a genome-wide association study and consecutive genotyping of human leukocyte antigens (HLAs) and killer cell immunoglobulin-like receptors. An initial genome-wide association study was performed with 275 CD patients and 2369 controls from a Korean population. To validate the loci identified in the genome-wide association study, replication genotyping was performed in a different cohort of 242 CD patients and 1066 controls. Finally, high-resolution genotyping of HLA and killer cell immunoglobulin-like receptor was performed. Four susceptibility loci, a promoter region in tumor necrosis factor (ligand) superfamily member (TNFSF15) and 3 independent regions in HLAs, showed significant associations with CD. Among them, rs114985235 in the intergenic region between HLA-B and HLA-C showed the strongest association, with an increased risk of CD (P = 8.71 × 10; odds ratio, 2.25). HLA typing in this region showed HLA-C*01 to be responsible for the association of CD among 43 HLA-B and HLA-C genotypes identified in the Korean population. However, the interaction of HLA-C with killer cell immunoglobulin-like receptor had little effect on the development of CD. We newly identified HLA-C*01 as a prominent CD-susceptibility HLA allotype in the Korean population. In addition, these results confirm that genetic variations in immune response genes, such as HLAs and TNFSF15, are important host factors for the pathogenesis of CD.
Publication Date: 2016-02-19
Journal: Inflammatory bowel diseases


tnfsf2(3)

A hospital-based study of clinical and genetic features of Crohn's disease.
The aim of this study was to gain a better understanding of the current incidence of Crohn's disease (CD) in Taiwan and examine its clinical/genetic characteristics because there has been a trend toward increased diagnosis in the Asia-Pacific area. The genetic background seen in CD cases in Taiwan seems to be different from that in Western countries. By reviewing the database in the National Taiwan University Hospital, CD patients were identified by clinical, endoscopic, and imaging findings. The clinical characteristics were recorded and analyzed. DNA was extracted from the peripheral blood of patients after obtaining informed consent. Polymerase chain reaction was performed with specific primers followed by direct sequencing to determine the single-nucleotide polymorphisms ATG16L1, CCR6, IL12B, IL23R, LRRK2, TNFSF2, and TNFSF15 CD-associated genes. Clinical data from 110 CD patients were examined from 1988 to 2008, with a mean follow-up period of 4.5 years. There was a marked increase in new CD diagnosis, especially after 2004. Among the 110 patients, 71 men and 39 women, the age at diagnosis was 30.5±17.8 years (mean±standard deviation). Stenosis occurred in 33.6% (37 of 110) and 40.9% (45 of 110) of patients who underwent surgery. The mortality rate was 2.7%, all because of sepsis. Genetic analysis of 39 patients showed that ATG16L1 and TNFSF15 were associated with susceptibility to CD in Taiwan. Recently, the incidence of CD diagnosis in Taiwan has markedly increased. ATG16L1 and TNFSF15 are associated with CD in Taiwan.
Publication Date: 2011-09-21
Journal: Journal of the Formosan Medical Association = Taiwan yi zhi