PMID- 22405769
OWN - NLM
STAT- MEDLINE
DCOM- 20120516
LR  - 20151119
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 420
IP  - 1
DP  - 2012 Mar 30
TI  - Th2-inducing cytokines IL-4 and IL-33 synergistically elicit the expression of 
      transmembrane TNF-alpha on macrophages through the autocrine action of IL-6.
PG  - 114-8
LID - 10.1016/j.bbrc.2012.02.124 [doi]
AB  - Tumor necrosis factor-alpha (TNF-alpha) is a potent proinflammatory cytokine produced 
      predominantly by activated macrophages, and plays a central role in the 
      protective immunity against intracellular pathogens and the pathogenesis of 
      autoimmune and inflammatory diseases. While both the soluble and transmembrane 
      forms of TNF-alpha (sTNF-alpha and tmTNF-alpha) are biologically functional, the latter but 
      not the former acts as a receptor besides as a ligand, and transmit a retrograde 
      signal in a cell-to-cell contact manner. The production of TNF-alpha by macrophages 
      under Th2-type (allergic) inflammatory conditions has been ill defined, compared 
      to that under Th1-type inflammatory conditions. Here we examined the effect of 
      representative Th2-inducing cytokines IL-4 and IL-33 on the TNF-alpha expression in 
      macrophages. IL-4 induced the production of neither sTNF-alpha nor tmTNF-alpha while 
      IL-33 promoted the production of sTNF-alpha with no detectable tmTNF-alpha. Notably, the 
      combination of IL-4 and IL-33 elicited the tmTNF-alpha expression on macrophages, in 
      addition to the enhanced production of sTNF-alpha and IL-6. The IL-4/IL-33-elicited 
      tmTNF-alpha expression was not observed in IL-6-deficient macrophages, suggesting the 
      involvement of macrophage-derived IL-6 in the tmTNF-alpha expression. Indeed, the 
      stimulation of macrophages with the combination of IL-4 and IL-6 induced the 
      tmTNF-alpha expression with no detectable production of sTNF-alpha. Thus, IL-4 and IL-33 
      synergistically elicit the tmTNF-alpha expression on macrophages through the 
      autocrine action of IL-6.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Ogawa, Hiromi
AU  - Ogawa H
AD  - Department of Immune Regulation, Tokyo Medical and Dental University Graduate 
      School, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.
FAU - Mukai, Kaori
AU  - Mukai K
FAU - Kawano, Yohei
AU  - Kawano Y
FAU - Minegishi, Yoshiyuki
AU  - Minegishi Y
FAU - Karasuyama, Hajime
AU  - Karasuyama H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120303
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Il33 protein, mouse)
RN  - 0 (Interleukin-33)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 207137-56-2 (Interleukin-4)
SB  - IM
MH  - Animals
MH  - *Autocrine Communication
MH  - Cell Membrane/immunology
MH  - Interleukin-33
MH  - Interleukin-4/pharmacology/*physiology
MH  - Interleukin-6/genetics/*metabolism
MH  - Interleukins/pharmacology/*physiology
MH  - Macrophages/drug effects/*immunology
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Inbred C57BL
MH  - Th2 Cells/*immunology
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
EDAT- 2012/03/13 06:00
MHDA- 2012/05/17 06:00
CRDT- 2012/03/13 06:00
PHST- 2012/02/21 00:00 [received]
PHST- 2012/02/22 00:00 [accepted]
PHST- 2012/03/13 06:00 [entrez]
PHST- 2012/03/13 06:00 [pubmed]
PHST- 2012/05/17 06:00 [medline]
AID - S0006-291X(12)00383-X [pii]
AID - 10.1016/j.bbrc.2012.02.124 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2012 Mar 30;420(1):114-8. doi: 
      10.1016/j.bbrc.2012.02.124. Epub 2012 Mar 3.