PMID- 8752938
OWN - NLM
STAT- MEDLINE
DCOM- 19961107
LR  - 20181130
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 157
IP  - 2
DP  - 1996 Jul 15
TI  - Human fibroblasts express functional IL-2 receptors formed by the IL-2R alpha- 
      and beta-chain subunits: association of IL-2 binding with secretion of the 
      monocyte chemoattractant protein-1.
PG  - 851-7
AB  - Expression of IL-2R was examined on human fibroblasts isolated from different 
      tissues. By specific binding assay it is shown that [125I]IL-2 bound to 
      subconfluent adult bone marrow and embryonic skin and lung fibroblasts. The 
      presence of binding sites for IL-2 was also confirmed by immunofluorescence and 
      flow cytometry analysis using mAbs specific for the p55 IL-2R alpha (anti-CD25), 
      p75 IL-2R beta, and p64 IL-2R gamma subunits. Fibroblasts also constitutively 
      transcribed the genes coding for IL-2R alpha and IL-2R beta and accumulated their 
      respective mRNAs but failed to exhibit the IL-2R gamma-chain on the mRNA and 
      protein level. Although addition of IL-2 to fibroblast cultures did not 
      significantly alter growth kinetics of these cells, the IL-2R complex displayed 
      by fibroblasts appeared to be functional in that addition of IL-2 to these cells 
      led to enhanced expression of the JE gene coding for the monocyte chemoattractant 
      protein-1 (MCP-1). Enhancement of fibroblast MCP-1/JE gene expression by IL-2 
      appeared to result from delayed MCP-1/JE mRNA decay rather than as a consequence 
      of an acceleration of the MCP-1/JE gene transcription rate. IL-2 had, however, no 
      effect on the expression of other cytokine genes including IL-1, IL-5, IL-6, 
      IL-7, IL-8, IL-9, granulocyte-macrophage-CSF, macrophage-CSF or TNF. These 
      observations suggest that the range of cellular targets of IL-2 is broader than 
      originally appreciated. IL-2 may thus serve to integrate fibroblasts and 
      monocytes into a coordinated response of the connective tissue initiated by T 
      lymphocytes.
FAU - Gruss, H J
AU  - Gruss HJ
AD  - Department of Internal Medicine III, University of Ulm Medical Center, Germany.
FAU - Scott, C
AU  - Scott C
FAU - Rollins, B J
AU  - Rollins BJ
FAU - Brach, M A
AU  - Brach MA
FAU - Herrmann, F
AU  - Herrmann F
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-2)
RN  - 0 (Iodine Radioisotopes)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Interleukin-2)
RN  - 62031-54-3 (Fibroblast Growth Factors)
SB  - IM
MH  - Adult
MH  - Base Sequence
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Cytokines/genetics
MH  - Fibroblast Growth Factors/physiology
MH  - Fibroblasts/*metabolism
MH  - Gene Expression Regulation/immunology
MH  - Humans
MH  - Interleukin-2/*metabolism/pharmacology
MH  - Iodine Radioisotopes
MH  - Molecular Sequence Data
MH  - Protein Binding/immunology
MH  - RNA, Messenger/biosynthesis/drug effects
MH  - Receptors, Interleukin-2/*biosynthesis/genetics/*physiology
EDAT- 1996/07/15 00:00
MHDA- 1996/07/15 00:01
CRDT- 1996/07/15 00:00
PHST- 1996/07/15 00:00 [pubmed]
PHST- 1996/07/15 00:01 [medline]
PHST- 1996/07/15 00:00 [entrez]
PST - ppublish
SO  - J Immunol. 1996 Jul 15;157(2):851-7.