|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0018956,
umls-concept:C0021761,
umls-concept:C0024432,
umls-concept:C0033268,
umls-concept:C0035820,
umls-concept:C0077503,
umls-concept:C0143630,
umls-concept:C0205195,
umls-concept:C0205314,
umls-concept:C0591833,
umls-concept:C0679622,
umls-concept:C1419030,
umls-concept:C1420280,
umls-concept:C1456820,
umls-concept:C1533691,
umls-concept:C2349975
|
|
pubmed:issue |
5
|
|
pubmed:dateCreated |
1994-9-28
|
|
pubmed:abstractText |
Tumor necrosis factor-alpha (TNF-alpha) is a bifunctional regulator of hematopoiesis, and its cellular responses are mediated by two distinct cell surface receptors. TNF-alpha generally inhibits the growth of primitive murine hematopoietic progenitor cells (Lin-Scal+) in response to multiple cytokine combinations, and the p75 TNF receptor is essential in signaling such inhibition. In the present study we show the reverse phenomenon in that TNF-alpha on the same progenitor cell population in combination with stem cell factor (SCF) and interleukin-7 (IL-7) through the p55 TNF receptor can recruit additional progenitors to proliferate. In contrast, TGF-beta 1, another bifunctional regulator of hematopoietic progenitor cell growth, completely blocked SCF plus IL-7-induced proliferation. TNF-alpha increased the number of responding progenitors, as well as the size of the colonies formed. The synergistic effects of TNF-alpha were seen at the single cell level, suggesting that its effects are directly mediated. Finally, whereas SCF plus IL-7 promoted primarily granulopoiesis, the addition of TNF-alpha switched the differentiation toward the production of almost exclusively macrophages.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
AIM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Sep
|
|
pubmed:issn |
0006-4971
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:day |
1
|
|
pubmed:volume |
84
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
1528-33
|
|
pubmed:dateRevised |
2006-11-15
|
|
pubmed:meshHeading |
pubmed-meshheading:7520777-Animals,
pubmed-meshheading:7520777-Bone Marrow Cells,
pubmed-meshheading:7520777-Cell Adhesion Molecules,
pubmed-meshheading:7520777-Cell Differentiation,
pubmed-meshheading:7520777-Cell Division,
pubmed-meshheading:7520777-Cells, Cultured,
pubmed-meshheading:7520777-Dose-Response Relationship, Drug,
pubmed-meshheading:7520777-Drug Synergism,
pubmed-meshheading:7520777-Hematopoietic Cell Growth Factors,
pubmed-meshheading:7520777-Hematopoietic Stem Cells,
pubmed-meshheading:7520777-Humans,
pubmed-meshheading:7520777-Interleukin-7,
pubmed-meshheading:7520777-Kinetics,
pubmed-meshheading:7520777-Macrophages,
pubmed-meshheading:7520777-Mice,
pubmed-meshheading:7520777-Mice, Inbred C57BL,
pubmed-meshheading:7520777-Rats,
pubmed-meshheading:7520777-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:7520777-Recombinant Proteins,
pubmed-meshheading:7520777-Stem Cell Factor,
pubmed-meshheading:7520777-Tumor Necrosis Factor-alpha
|
|
pubmed:year |
1994
|
|
pubmed:articleTitle |
Tumor necrosis factor-alpha (TNF-alpha) potently enhances in vitro macrophage production from primitive murine hematopoietic progenitor cells in combination with stem cell factor and interleukin-7: novel stimulatory role of p55 TNF receptors.
|
|
pubmed:affiliation |
Department of Immunology, Norwegian Radium Hospital, Montebello.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
