12023397

Source:http://linkedlifedata.com/resource/pubmed/id/12023397

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Predicate	Object
rdf:type	pubmed:Citation
lifeskim:mentions	umls-concept:C0030705, umls-concept:C0033268, umls-concept:C0085236, umls-concept:C0242633, umls-concept:C0271510, umls-concept:C0332157, umls-concept:C0700624, umls-concept:C0806987, umls-concept:C1098076, umls-concept:C1998811
pubmed:issue	11
pubmed:dateCreated	2002-5-22
pubmed:abstractText	Diesel exhausts and their associated organic compounds may be involved in the recent increase in the prevalence of allergic disorders, through their ability to favor a type 2 immune response. Type 2 T cells have been shown to be preferentially recruited by the chemokines eotaxin (CCL11), macrophage-derived chemokine (MDC, CCL22), and thymus activation-regulated chemokine (CCL17) through their interaction with CCR3 and CCR4, respectively, whereas type 1 T cells are mainly recruited by IFN-gamma-induced protein-10 (CXCL10) through CXCR3 binding. The aim of the study was to evaluate the effect of diesel exposure on the expression of chemokines involved in type 1 and 2 T cell recruitment. PBMC and alveolar macrophages from house dust mite allergic patients were incubated with combinations of diesel extracts and Der p 1 allergen, and chemokine production was analyzed. Diesel exposure alone decreased the constitutive IP-10 production, while it further augmented allergen-induced MDC production, resulting in a significantly increased capacity to chemoattract human Th2, but not Th1 clones. Inhibition experiments with anti-type 1 or type 2 cytokine Abs as well as cytokine mRNA kinetic evaluation showed that the chemokine variations were not dependent upon IL-4, IL-13, or IFN-gamma expression. In contrast, inhibition of the B7:CD28 pathway using a CTLA-4-Ig fusion protein completely inhibited diesel-dependent increase of allergen-induced MDC production. This inhibition was mainly dependent upon the CD86 pathway and to a lesser extent upon the CD80 pathway. These results suggest that the exposure to diesel exhausts and allergen may likely amplify a deleterious type 2 immune response via a differential regulation of chemokine production through the CD28 pathway.
pubmed:language	eng
pubmed:journal	http://linkedlifedata.com/resource/pubmed/journal/2985117R
pubmed:citationSubset	AIM
pubmed:chemical	http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD28, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD80, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Dermatophagoides, http://linkedlifedata.com/resource/pubmed/chemical/CCL22 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL22, http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CXCL10, http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CC, http://linkedlifedata.com/resource/pubmed/chemical/Chemokines, CXC, http://linkedlifedata.com/resource/pubmed/chemical/Glycoproteins, http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Chemokine, http://linkedlifedata.com/resource/pubmed/chemical/Vehicle Emissions
pubmed:status	MEDLINE
pubmed:month	Jun
pubmed:issn	0022-1767
pubmed:author	pubmed-author:FahyOlivierO, pubmed-author:LassallePhilippeP, pubmed-author:PèneJérômeJ, pubmed-author:SénéchalStéphanieS, pubmed-author:ScherpereelArnaudA, pubmed-author:TonnelAndré-BernardAB, pubmed-author:TsicopoulosAnneA, pubmed-author:WallaertBenoîtB, pubmed-author:YsselHansH
pubmed:issnType	Print
pubmed:day	1
pubmed:volume	168
pubmed:owner	NLM
pubmed:authorsComplete	Y
pubmed:pagination	5912-9
pubmed:dateRevised	2007-11-15
pubmed:meshHeading	pubmed-meshheading:12023397-Antigens, CD28, pubmed-meshheading:12023397-Antigens, CD80, pubmed-meshheading:12023397-Antigens, Dermatophagoides, pubmed-meshheading:12023397-Chemokine CCL22, pubmed-meshheading:12023397-Chemokine CXCL10, pubmed-meshheading:12023397-Chemokines, pubmed-meshheading:12023397-Chemokines, CC, pubmed-meshheading:12023397-Chemokines, CXC, pubmed-meshheading:12023397-Chemotaxis, Leukocyte, pubmed-meshheading:12023397-Glycoproteins, pubmed-meshheading:12023397-Humans, pubmed-meshheading:12023397-Hypersensitivity, pubmed-meshheading:12023397-Leukocytes, Mononuclear, pubmed-meshheading:12023397-Macrophages, Alveolar, pubmed-meshheading:12023397-RNA, Messenger, pubmed-meshheading:12023397-Receptors, Chemokine, pubmed-meshheading:12023397-Th2 Cells, pubmed-meshheading:12023397-Vehicle Emissions
pubmed:year	2002
pubmed:articleTitle	Diesel exposure favors Th2 cell recruitment by mononuclear cells and alveolar macrophages from allergic patients by differentially regulating macrophage-derived chemokine and IFN-gamma-induced protein-10 production.
pubmed:affiliation	Institut National de la Santé et de la Recherche Médicale Unité 416, Institut Pasteur de Lille, Lille, France.
pubmed:publicationType	Journal Article, Research Support, Non-U.S. Gov't