Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1993-1-8
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0950-3536
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
703-21
pubmed:dateRevised
2007-11-14
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
pubmed:year
1992
pubmed:articleTitle
Transforming growth factor beta and interleukin-1: a paradigm for opposing regulation of haemopoiesis.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review