{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,6]],"date-time":"2026-02-06T03:24:23Z","timestamp":1770348263288,"version":"3.49.0"},"reference-count":44,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2012,8,28]],"date-time":"2012-08-28T00:00:00Z","timestamp":1346112000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Helicobacter"],"published-print":{"date-parts":[[2013,2]]},"abstract":"Abstract<\/jats:title>Background<\/jats:title>H<\/jats:styled-content>elicobacter pylori<\/jats:italic> infects approximately 50% of the world population. Among the infected individuals, only 10\u201320% develop peptic ulcers and <3% progress to gastric cancer (GC<\/jats:styled-content>). Th1\u2010predominant immune responses have been suggested to underlie H<\/jats:styled-content>.\u00a0pylori<\/jats:italic>\u2010induced gastric diseases. However, the reason for a strong inter\u2010individual variation of susceptibility and course of the disease is currently far from being understood. It has been shown that H<\/jats:styled-content>.\u00a0pylori<\/jats:italic> stimulates the host's Toll\u2010like receptor (TLR<\/jats:styled-content>) 2\/1 complex. Furthermore, the single nucleotide polymorphism (SNP<\/jats:styled-content>) I602S of TLR<\/jats:styled-content>1 alters the inflammatory cytokine response of monocytes. Therefore, we hypothesized an association of this TLR<\/jats:styled-content>1 SNP<\/jats:styled-content> with H<\/jats:styled-content>.\u00a0pylori<\/jats:italic>\u2010mediated gastric pathologies.<\/jats:p><\/jats:sec>Materials and Methods<\/jats:title>Subjects with different TLR<\/jats:styled-content>1 genotypes were analyzed for their IFN<\/jats:styled-content>\u2010\u03b3 response of NK<\/jats:styled-content>\u2010 and T\u2010cells. We further genotyped 548 patients with gastric diseases for this SNP<\/jats:styled-content> and compared patients with gastritis with those having ulcer, and patients with high\u2010risk gastritis versus patients with GC<\/jats:styled-content>.<\/jats:p><\/jats:sec>Results<\/jats:title>Homozygous 602S allele carriers exhibited impaired in vitro IFN<\/jats:styled-content>\u2010\u03b3 responses to the TLR<\/jats:styled-content>2\/1 agonist Pam3<\/jats:sub>CSK<\/jats:styled-content>4<\/jats:sub>. The TLR<\/jats:styled-content>1 I602S SNP<\/jats:styled-content> is significantly associated with GC<\/jats:styled-content> (p<\/jats:italic>\u00a0=\u00a0.002) and gastric ulcer (p<\/jats:italic>\u00a0=\u00a0.051). Odds ratios showed significantly reduced risk regarding GC<\/jats:styled-content> and peptic ulcer for the homozygous mutated genotype. The odds ratios were 0.4 (95% CI<\/jats:styled-content>, 0.22\u20130.72) and 0.588 (95% CI<\/jats:styled-content>, 0.35\u20131.00), respectively.<\/jats:p><\/jats:sec>Conclusion<\/jats:title>In conclusion, our results suggest that the nonfunctional TLR<\/jats:styled-content>1 602S\/S genotype is associated with a reduced risk of H<\/jats:styled-content>.\u00a0pylori<\/jats:italic>\u2010induced gastric diseases, probably via diminished Th1 responses.<\/jats:p><\/jats:sec>","DOI":"10.1111\/hel.12001","type":"journal-article","created":{"date-parts":[[2012,8,29]],"date-time":"2012-08-29T03:49:11Z","timestamp":1346212151000},"page":"13-21","source":"Crossref","is-referenced-by-count":32,"title":["A Frequent Toll\u2010Like Receptor 1 Gene Polymorphism Affects NK<\/scp>\u2010 and T\u2010cell IFN<\/scp>\u2010\u03b3 Production and is Associated with Helicobacter pylori<\/i>\u2010induced Gastric Disease"],"prefix":"10.1111","volume":"18","author":[{"given":"Chin\u2010An","family":"Yang","sequence":"first","affiliation":[{"name":"Institute of Medical Immunology CVK Charit\u00e9\u2010University Medical Center Berlin Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carmen","family":"Scheibenbogen","sequence":"additional","affiliation":[{"name":"Institute of Medical Immunology CVK Charit\u00e9\u2010University Medical Center Berlin Germany"},{"name":"Berlin\u2010Brandenburg Center for Regenerative Therapies (BCRT), Charit\u00e9 Campus Virchow Klinikum Berlin Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Sandra","family":"Bauer","sequence":"additional","affiliation":[{"name":"Institute of Medical Immunology CVK Charit\u00e9\u2010University Medical Center Berlin Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christoph","family":"Kleinle","sequence":"additional","affiliation":[{"name":"Institute for Microbiology and Hygiene CBF, Charit\u00e9\u2010University Medical Center Berlin Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Thomas","family":"Wex","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, Hepatology and Infectious Diseases Otto\u2010von\u2010Guericke University Magdeburg Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jan","family":"Bornschein","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, Hepatology and Infectious Diseases Otto\u2010von\u2010Guericke University Magdeburg Germany"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Peter","family":"Malfertheiner","sequence":"additional","affiliation":[{"name":"Department of Gastroenterology, Hepatology and Infectious Diseases Otto\u2010von\u2010Guericke University Magdeburg 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