Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2006-2-22
pubmed:abstractText
We found a population of nonlymphoid cells expressing both CD4 and CD8 in peripheral blood mononuclear cells (PBMCs) of human T-cell leukemia virus type-I pX transgenic rats with autoimmune diseases. These cells, which showed a monocytic phenotype, were also found in wild-type rats, and their number increased by adjuvant-assisted immunization. GM-CSF increased the number of these double-positive (DP) monocytes in PBMCs. Consistent with the idea that DP monocytes differentiate into DP macrophages at sites of inflammation, we found infiltration of DP macrophages at the site of myosin-induced myocarditis in wild-type rats; these cells exhibited a T-helper 1 (Th1)-type cytokine/chemokine profile and expressed high levels of Fas ligand, perforin, granzyme B, and NKR-P2 (rat orthologue of human NKG2D). Adoptive transfer of GFP-positive spleen cells confirmed hematogenous origin of DP macrophages. DP monocytes had a cytotoxic phenotype similar to DP macrophages, indicating that this phenotypic specialization occurred before entry into a tissue. In line with this, DP monocytes killed tumor cells in vitro. Combined evidence indicates that certain inflammatory stimuli that induce GM-CSF trigger the expansion of a population of DP monocytes with a cytotoxic phenotype and that these cells differentiate into macrophages at inflammatory sites. Interestingly, human PBMCs also contain DP monocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Adjuvants, Immunologic, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD8, http://linkedlifedata.com/resource/pubmed/chemical/Cytokines, http://linkedlifedata.com/resource/pubmed/chemical/GZMB protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Granzymes, http://linkedlifedata.com/resource/pubmed/chemical/Gzmb protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins, http://linkedlifedata.com/resource/pubmed/chemical/NKR-P2 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Perforin, http://linkedlifedata.com/resource/pubmed/chemical/Pore Forming Cytotoxic Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic, http://linkedlifedata.com/resource/pubmed/chemical/Serine Endopeptidases
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
107
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2004-12
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:16269616-Adjuvants, Immunologic, pubmed-meshheading:16269616-Animals, pubmed-meshheading:16269616-Animals, Genetically Modified, pubmed-meshheading:16269616-Antigens, CD4, pubmed-meshheading:16269616-Antigens, CD8, pubmed-meshheading:16269616-Cell Differentiation, pubmed-meshheading:16269616-Cell Movement, pubmed-meshheading:16269616-Cytokines, pubmed-meshheading:16269616-Granzymes, pubmed-meshheading:16269616-Human T-lymphotropic virus 1, pubmed-meshheading:16269616-Humans, pubmed-meshheading:16269616-Inflammation, pubmed-meshheading:16269616-Lectins, C-Type, pubmed-meshheading:16269616-Macrophage Activation, pubmed-meshheading:16269616-Macrophages, pubmed-meshheading:16269616-Membrane Glycoproteins, pubmed-meshheading:16269616-Neoplasms, pubmed-meshheading:16269616-Perforin, pubmed-meshheading:16269616-Pore Forming Cytotoxic Proteins, pubmed-meshheading:16269616-Rats, pubmed-meshheading:16269616-Receptors, Immunologic, pubmed-meshheading:16269616-Serine Endopeptidases, pubmed-meshheading:16269616-Transgenes
pubmed:year
2006
pubmed:articleTitle
CD4+/CD8+ macrophages infiltrating at inflammatory sites: a population of monocytes/macrophages with a cytotoxic phenotype.
pubmed:affiliation
Department of Pathology/Pathophysiology, Division of Pathophysiological Science, Hokkaido University Graduate School of Medicine, Kita-15, Nishi-7, Kita-ku, Sapporo 060-8638, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't