Pubmed output: What's new for 'JKB

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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Saturday, 2010 Jun 12
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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PubMed Results

Items 1 - 4 of 4

1.	N Engl J Med. 2010 Jun 3;362(22):2135; author reply 2136. Macrophages in Hodgkin's lymphoma. Pazianas M. Comment on: N Engl J Med. 2010 Mar 11;362(10):875-85.
	PMID: 20527079 [PubMed - indexed for MEDLINE]
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2.	N Engl J Med. 2010 Jun 3;362(22):2135-6; author reply 2136. Macrophages in Hodgkin's lymphoma. Kadin ME. Comment on: N Engl J Med. 2010 Mar 11;362(10):875-85.
	PMID: 20527059 [PubMed - indexed for MEDLINE]
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3.	N Engl J Med. 2010 Jun 3;362(22):2135; author reply 2136. Macrophages in Hodgkin's lymphoma. Tsubokura M, Kodama Y, Kami M. Comment on: N Engl J Med. 2010 Mar 11;362(10):875-85.
	PMID: 20519687 [PubMed - indexed for MEDLINE]
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4.	N Engl J Med. 2010 Jun 3;362(22):2092-101. Epub 2010 May 19. CISH and susceptibility to infectious d iseases. Khor CC, Vannberg FO, Chapman SJ, Guo H, Wong SH, Walley AJ, Vukcevic D, Rautanen A, Mills TC, Chang KC, Kam KM, Crampin AC, Ngwira B, Leung CC, Tam CM, Chan CY, Sung JJ, Yew WW, Toh KY, Tay SK, Kwiatkowski D, Lienhardt C, Hien TT, Day NP, Peshu N, Marsh K, Maitland K, Scott JA, Williams TN, Berkley JA, Floyd S, Tang NL, Fine PE, Goh DL, Hill AV. The Wellcome Trust Centre for Human Genetics, University of Oxford, Oxford, United Kingdom. khorcc@gis.a-star.edu.sg Abstract BACKGROUND: The interleukin-2-mediated immune response is critical for host defense against infectious pathogens. Cytokine-inducible SRC homology 2 (SH2) domain protein (CISH), a suppressor of cytokine signaling, controls interleukin-2 signaling. METHODS: Using a case-control design, we tested for an association between CISH polymorphisms and susceptibility to major infectious diseases (bacteremia, tuberculosis, and severe malaria) in blood samples from 8402 persons in Gambia, Hong Kong, Kenya, Malawi, and Vietnam. We had previously tested 20 other immune-related genes in one or more of these sample collections. RESULTS: We observed associations between variant alleles of multiple CISH polymorphisms and increased susceptibility to each infectious disease in each of the study populations. When all five single-nucleotide polymorphisms (SNPs) (at positions -639, -292, -163, +1320, and +3415 [all relative to CISH]) within the CISH-associated locus were considered together in a multiple-SNP score, we found an association between CISH genetic variants and susceptibility to bacteremia, malaria, and tuberculosis (P=3.8x10(-11) for all comparisons), with -292 accounting for most of the association signal (P=4.58x10(-7)). Peripheral-blood mononuclear cells obtained from adult subjects carrying the -292 variant, as compared with wild-type cells, showed a muted response to the stimulation of interleukin-2 production--that is, 25 to 40% less CISH expression. CONCLUSIONS: Variants of CISH are associated with susceptibility to diseases caused by diverse infectious pathogens, suggesting that negative regulators of cytokine signaling have a role in immunity against various infectious diseases. The overall risk of one of these infectious diseases was increased by at least 18% among persons carrying the variant CISH alleles. 2010 Massachusetts Medical Society
	PMID: 20484391 [PubMed - indexed for MEDLINE]
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