Linked Life Data

11390447

Source:http://linkedlifedata.com/resource/pubmed/id/11390447

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2001-6-6
pubmed:abstractText
Macrophages and dendritic cells (DC) play an essential role in the initiation and maintenance of immune response to pathogens. To analyze early interactions between Mycobacterium tuberculosis (Mtb) and immune cells, human peripheral blood monocyte-derived macrophages (MDM) and monocyte-derived dendritic cells (MDDC) were infected with Mtb. Both cells were found to internalize the mycobacteria, resulting in the activation of MDM and maturation of MDDC as reflected by enhanced expression of several surface Ags. After Mtb infection, the proinflammatory cytokines TNF-alpha, IL-1, and IL-6 were secreted mainly by MDM. As regards the production of IFN-gamma-inducing cytokines, IL-12 and IFN-alpha, was seen almost exclusively from infected MDDC, while IL-18 was secreted preferentially by macrophages. Moreover, Mtb-infected MDM also produce the immunosuppressive cytokine IL-10. Because IL-10 is a potent inhibitor of IL-12 synthesis from activated human mononuclear cells, we assessed the inhibitory potential of this cytokine using soluble IL-10R. Neutralization of IL-10 restored IL-12 secretion from Mtb-infected MDM. In line with these findings, supernatants from Mtb-infected MDDC induced IFN-gamma production by T cells and enhanced IL-18R expression, whereas supernatants from MDM failed to do that. Neutralization of IFN-alpha, IL-12, and IL-18 activity in Mtb-infected MDDC supernatants by specific Abs suggested that IL-12 and, to a lesser extent, IFN-alpha and IL-18 play a significant role in enhancing IFN-gamma synthesis by T cells. During Mtb infection, macrophages and DC may have different roles: macrophages secrete proinflammatory cytokines and induce granulomatous inflammatory response, whereas DC are primarily involved in inducing antimycobacterial T cell immune response.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
166
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7033-41
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11390447-Biological Markers, pubmed-meshheading:11390447-Cell Differentiation, pubmed-meshheading:11390447-Cells, Cultured, pubmed-meshheading:11390447-Cytokines, pubmed-meshheading:11390447-Dendritic Cells, pubmed-meshheading:11390447-Gene Expression Regulation, pubmed-meshheading:11390447-Humans, pubmed-meshheading:11390447-Interferon-gamma, pubmed-meshheading:11390447-Interleukin-18, pubmed-meshheading:11390447-Interleukin-18 Receptor alpha Subunit, pubmed-meshheading:11390447-Kinetics, pubmed-meshheading:11390447-Lymphocyte Activation, pubmed-meshheading:11390447-Macrophage Activation, pubmed-meshheading:11390447-Macrophages, pubmed-meshheading:11390447-Mycobacterium tuberculosis, pubmed-meshheading:11390447-Receptors, Interleukin, pubmed-meshheading:11390447-Receptors, Interleukin-18, pubmed-meshheading:11390447-T-Lymphocytes, pubmed-meshheading:11390447-Up-Regulation
pubmed:year
2001
pubmed:articleTitle
Infection of human macrophages and dendritic cells with Mycobacterium tuberculosis induces a differential cytokine gene expression that modulates T cell response.
pubmed:affiliation
Laboratories of. Immunology and Bacteriology and Medical Mycology, Istituto Superiore di Sanità, Rome, Italy. Department of Virology, National Public Health Institute, Helsinki, Finland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't