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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
1993-1-8
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pubmed:abstractText |
The polypeptide cytokines, IL-1 and TGF-beta affect nearly every tissue and cell type in the body. IL-1 is the prototype of the proinflammatory molecule while TGF-beta is essentially anti-inflammatory. IL-1 is part of the cascade of cytokines that are produced during microbial invasion or bodily injury and enhance a variety of host responses, particularly in the immunological and haemopoietic systems, while TGF-beta acts as an inhibitor of these responses. At several levels, IL-1 and TGF-beta act in opposition to one another. IL-1 stimulates the expression of many genes in lymphoid and marrow stromal cells that stimulate haemopoietic cell growth and differentiation, while TGF-beta inhibits these IL-1 mediated effects. Also, TGF-beta stimulates secretion of the IL-1Ra. In addition, IL-1 induces the cell surface expression of cytokine receptors on lymphoid and haemopoietic cells, while TGF-beta dramatically inhibits the cell surface expression of these receptors, including the IL-1 receptor. Finally, IL-1 augments lymphoid and haemopoietic cell growth and TGF-beta potently inhibits this proliferation. The interactions of these cytokines serve to illustrate that the net balance of stimulatory and inhibitory signals determines the fate of a given cell which may be responsible for regulating homeostatic cell growth (Figure 1). Thus, the regulation of cytokine production and/or antagonism of their effects continues to be a therapeutic goal in the treatment of many diseases.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Hematopoietic Cell Growth Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cell Surface,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0950-3536
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
5
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
703-21
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1333850-Animals,
pubmed-meshheading:1333850-Bone Marrow Cells,
pubmed-meshheading:1333850-Cell Cycle,
pubmed-meshheading:1333850-Cell Differentiation,
pubmed-meshheading:1333850-Cell Division,
pubmed-meshheading:1333850-Colony-Forming Units Assay,
pubmed-meshheading:1333850-Cytokines,
pubmed-meshheading:1333850-Gene Expression Regulation,
pubmed-meshheading:1333850-Hematopoiesis,
pubmed-meshheading:1333850-Hematopoietic Cell Growth Factors,
pubmed-meshheading:1333850-Hematopoietic Stem Cells,
pubmed-meshheading:1333850-Humans,
pubmed-meshheading:1333850-Interleukin-1,
pubmed-meshheading:1333850-Leukemia,
pubmed-meshheading:1333850-Lymphocyte Activation,
pubmed-meshheading:1333850-Lymphoma,
pubmed-meshheading:1333850-Mice,
pubmed-meshheading:1333850-Models, Biological,
pubmed-meshheading:1333850-Organ Culture Techniques,
pubmed-meshheading:1333850-Receptors, Cell Surface,
pubmed-meshheading:1333850-T-Lymphocytes,
pubmed-meshheading:1333850-Transforming Growth Factor beta
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pubmed:year |
1992
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pubmed:articleTitle |
Transforming growth factor beta and interleukin-1: a paradigm for opposing regulation of haemopoiesis.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review
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