PMID- 9079810
OWN - NLM
STAT- MEDLINE
DCOM- 19970429
LR  - 20071115
IS  - 0014-2980 (Print)
IS  - 0014-2980 (Linking)
VI  - 27
IP  - 3
DP  - 1997 Mar
TI  - Regulation of I-309 gene expression in human monocytes by endogenous 
      interleukin-1.
PG  - 687-94
AB  - Activated human monocytes are a source of numerous beta-chemokines. The present 
      study was conducted to determine whether these cells produce the human 
      beta-chemokine I-309 and to compare the induction requirements of I-309 to those 
      of other beta-chemokines. We demonstrate that appropriately stimulated 
      adherence-purified human peripheral blood monocytes express I-309 transcripts and 
      secreted I-309 protein. Two stimuli, immobilized IgG and lipopolysaccharide 
      (LPS), synergize strongly to induce I-309 gene expression. We further demonstrate 
      that the production of endogenous interleukin (IL)-1alpha plays a crucial role in 
      I-309 induction. Thus, neutralization of endogenous IL-1alpha using an 
      anti-IL-1alpha antiserum inhibits the induction of I-309 transcripts in response 
      to stimulation with immobilized IgG and LPS, and exogenous IL-1alpha or IL-1beta 
      induces I-309 transcripts in monocytes stimulated with immobilized IgG. 
      Immobilized IgG and LPS have the opposite effect on monocyte chemoattractant 
      protein-1 (MCP-1) gene expression, in that the induction observed with either 
      stimulus alone is diminished using the two stimuli in combination. Furthermore, 
      endogenous and exogenous IL-1 can be either stimulatory or inhibitory for MCP-1 
      gene expression depending on other signals delivered to the monocytes. 
      Immobilized IgG and LPS synergize to induce macrophage inflammatory 
      protein-1alpha transcripts, but endogenous IL-1 does not play a significant role. 
      Thus, each of these beta-chemokine genes is under distinct regulatory control in 
      human monocytes.
FAU - Selvan, R S
AU  - Selvan RS
AD  - Department of Immunology, Duke University Medical Center, Durham, NC 27710, USA. 
      selva001@mc.duke.edu
FAU - Zhou, L J
AU  - Zhou LJ
FAU - Krangel, M S
AU  - Krangel MS
LA  - eng
PT  - Journal Article
PL  - Germany
TA  - Eur J Immunol
JT  - European journal of immunology
JID - 1273201
RN  - 0 (CCL1 protein, human)
RN  - 0 (Chemokine CCL1)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemokines)
RN  - 0 (Chemokines, CC)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Interleukin-1)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Cell Adhesion
MH  - Cells, Cultured
MH  - Chemokine CCL1
MH  - Chemokine CCL2/genetics
MH  - Chemokine CCL4
MH  - Chemokines/*genetics
MH  - *Chemokines, CC
MH  - Gene Expression
MH  - Humans
MH  - Immunoglobulin G/pharmacology
MH  - Interleukin-1/physiology
MH  - Lipopolysaccharides/pharmacology
MH  - Macrophage Inflammatory Proteins/genetics
MH  - Monocytes/*physiology
MH  - RNA, Messenger/genetics
MH  - Transcription, Genetic
EDAT- 1997/03/01 00:00
MHDA- 1997/03/01 00:01
CRDT- 1997/03/01 00:00
PHST- 1997/03/01 00:00 [pubmed]
PHST- 1997/03/01 00:01 [medline]
PHST- 1997/03/01 00:00 [entrez]
AID - 10.1002/eji.1830270317 [doi]
PST - ppublish
SO  - Eur J Immunol. 1997 Mar;27(3):687-94. doi: 10.1002/eji.1830270317.