Linked Life Data

12538673

Source:http://linkedlifedata.com/resource/pubmed/id/12538673

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2003-1-22
pubmed:abstractText
We recently reported that dendritic cells (DC) infected with Mycobacterium tuberculosis (Mtb) produce Th1/IFN-gamma-inducing cytokines, IFN-alpha beta and IL-12. In the present article, we show that maturing Mtb-infected DC express high levels of CCR7 and they become responsive to its ligand CCL21. Conversely, CCR5 expression was rapidly lost from the cell surface following Mtb infection. High levels of CCL3 and CCL4 were produced within 8 h after infection, which is likely to account for the observed CCR5 down-modulation on Mtb-infected DC. In addition, Mtb infection stimulated the secretion of CXCL9 and CXCL10. Interestingly, the synthesis of CXCL10 was mainly dependent on the Mtb-induced production of IFN-alpha beta. Indeed, IFN-alpha beta neutralization down-regulated CXCL10 expression, whereas the expression of CXCL9 appeared to be unaffected. The chemotactic activity of the Mtb-infected DC supernatants was evaluated by migration assays using activated NK, CD4(+), and CD8(+) cells that expressed both CCR5 and CXCR3. Mtb-induced expression of CCL3, CCL4, CXCL9, and CXCL10 was involved in the stimulation of NK and T cell migration. In accordance with the data on the IFN-alpha beta-induced expression of CXCL10, neutralization of IFN-alpha beta significantly reduced the chemotactic activity of the supernatant from Mtb-infected DC. This indicates that IFN-alpha beta may modulate the immune response through the expression of CXCL10, which along with CXCL9, CCL3, and CCL4 participates in the recruitment and selective homing of activated/effector cells, which are known to accumulate at the site of Mtb infection and take part in the formation of the granulomas.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
170
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1174-82
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:12538673-CD4-Positive T-Lymphocytes, pubmed-meshheading:12538673-CD8-Positive T-Lymphocytes, pubmed-meshheading:12538673-Cell Differentiation, pubmed-meshheading:12538673-Cell Movement, pubmed-meshheading:12538673-Cells, Cultured, pubmed-meshheading:12538673-Chemokine CXCL10, pubmed-meshheading:12538673-Chemokines, pubmed-meshheading:12538673-Chemokines, CXC, pubmed-meshheading:12538673-Coculture Techniques, pubmed-meshheading:12538673-Dendritic Cells, pubmed-meshheading:12538673-Gene Expression Regulation, pubmed-meshheading:12538673-Humans, pubmed-meshheading:12538673-Interferon Type I, pubmed-meshheading:12538673-Killer Cells, Natural, pubmed-meshheading:12538673-Lymphocyte Activation, pubmed-meshheading:12538673-Mycobacterium tuberculosis, pubmed-meshheading:12538673-Receptors, Chemokine, pubmed-meshheading:12538673-T-Lymphocyte Subsets
pubmed:year
2003
pubmed:articleTitle
IFN-alpha beta released by Mycobacterium tuberculosis-infected human dendritic cells induces the expression of CXCL10: selective recruitment of NK and activated T cells.
pubmed:affiliation
Laboratory of Immunology, Istituto Superiore di Sanità, Rome, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't