PMID- 8240934
OWN - NLM
STAT- MEDLINE
DCOM- 19931229
LR  - 20061115
IS  - 0896-0623 (Print)
IS  - 0896-0623 (Linking)
VI  - 5
IP  - 3-4
DP  - 1993 May-Aug
TI  - Regulation of tumor necrosis factor-alpha receptors on macrophages: differences 
      between primary macrophages and transformed macrophage cell lines.
PG  - 158-64
AB  - Macrophages are a pivotal cell in the production of a variety of cytokines. In 
      addition, macrophages express receptors on their surface which allows them to act 
      as target cells for cytokines. The regulation of both cytokine production and 
      cytokine receptor expression in macrophages may play a key role in modulating the 
      processes of inflammation, injury, and repair. In this report we have studied the 
      regulation of macrophage receptors for tumor necrosis factor-alpha (TNF alpha) on 
      rat bone marrow-derived macrophages, rat alveolar macrophages, human 
      monocyte-derived macrophages, and the human monocyte-like cell line, U937, by a 
      variety of immunomodulatory and inflammatory agents. U937 cells and rat and human 
      macrophages bound TNF alpha in a saturable process, with an affinity in each cell 
      type of approximately 1 nM. Following incubation with phorbol myristate acetate 
      for 60 min, TNF alpha binding to all cells was decreased. Interleukin-1 treatment 
      increased TNF alpha binding to human and rat macrophages. Interferon-gamma 
      treatment decreased receptor activity in both human and rat macrophages, but 
      increased TNF alpha binding to U937 cells. Treatment of human and rat macrophages 
      with endotoxin resulted in a rapid loss of TNF alpha binding, while endotoxin 
      treatment increased receptor expression in U937 cells. In all cases, receptor 
      regulation was the result of a change in receptor number. Finally, following 
      intraperitoneal injection of endotoxin, TNF alpha receptor expression was 
      down-regulated on alveolar lavage cells from rats.(ABSTRACT TRUNCATED AT 250 
      WORDS)
FAU - Welborn, M B
AU  - Welborn MB
AD  - Department of Veteran's Affairs, Nashville, TN.
FAU - Christman, J W
AU  - Christman JW
FAU - Shepherd, V L
AU  - Shepherd VL
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Reg Immunol
JT  - Regional immunology
JID - 9001013
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Cell Line, Transformed
MH  - Cells, Cultured
MH  - Down-Regulation
MH  - Humans
MH  - Lipopolysaccharides/toxicity
MH  - Macrophages/immunology/*metabolism
MH  - Macrophages, Alveolar/drug effects/metabolism
MH  - Rats
MH  - Receptors, Tumor Necrosis Factor/*metabolism
MH  - Toxemia/chemically induced/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 1993/05/01 00:00
MHDA- 1993/05/01 00:01
CRDT- 1993/05/01 00:00
PHST- 1993/05/01 00:00 [pubmed]
PHST- 1993/05/01 00:01 [medline]
PHST- 1993/05/01 00:00 [entrez]
PST - ppublish
SO  - Reg Immunol. 1993 May-Aug;5(3-4):158-64.