PMID- 11983693
OWN - NLM
STAT- MEDLINE
DCOM- 20020822
LR  - 20210206
IS  - 0021-9258 (Print)
IS  - 0021-9258 (Linking)
VI  - 277
IP  - 30
DP  - 2002 Jul 26
TI  - Opposite regulation of type II and III receptors for immunoglobulin G in mouse 
      glomerular mesangial cells and in the induction of anti-glomerular basement 
      membrane (GBM) nephritis.
PG  - 27535-44
AB  - We examined the capacity of mouse glomerular mesangial cells (MC) to express and 
      function through two different low affinity FcgammaRs, the activating FcgammaRIII 
      and the inhibitory FcgammaRII. Immunohistochemistry identified FcgammaRII as the 
      prominent FcgammaR in the kidney, and low levels of FcgammaRIIb2-specific mRNA 
      were also detected in primary cultures of growth-arrested MC. Activation by tumor 
      necrosis factor-alpha/interleukin-1beta induced substantial FcgammaRII expression 
      in proliferating MC. Importantly, however, stimulation with interferon-gamma 
      (IFN-gamma)/lipopolysaccharide or IFN-gamma alone resulted in a complete 
      down-regulation of FcgammaRII, which was accompanied by a strong increase in 
      FcRgamma chain mRNA and a surface appearance of FcgammaRIII. Activating 
      FcgammaRIII triggered mRNA synthesis for monocyte chemoattractant protein-1 
      (MCP-1), MCP-5, cytokine-induced neutrophil chemoattractant, and RANTES, whereas 
      FcgammaRIII-deficient MC failed to respond to immune complex (IC) activation as 
      shown by impaired production of MCP-1 mRNA/protein. In a passive model of acute 
      anti-glomerular basement membrane (GBM) nephritis, induction of FcgammaRIII and 
      suppression of FcgammaRII occurred in kidney tissues. Blockade of FcgammaRII, 
      when induced selectively in the kidney, resulted in enhanced inflammation. Taken 
      together, our results define a novel regulatory pathway with opposite regulation 
      of FcgammaRII (suppressed) and FcgammaRIII (induced) by IFN-gamma on MCs in vitro 
      and anti-GBM IgG in vivo. Herein is provided the first evidence that glomerular 
      FcgammaRII plays an important immunoregulatory role in the initiation of IC 
      glomerulonephritis.
FAU - Radeke, Heinfried H
AU  - Radeke HH
AD  - Department of Clinical Immunology and Institute of Pharmacology, Medical School 
      of Hannover, Carl-Neuberg-Strasse 1, 30625 Hannover, Germany.
FAU - Janssen-Graalfs, Iska
AU  - Janssen-Graalfs I
FAU - Sowa, Eveline N
AU  - Sowa EN
FAU - Chouchakova, Nelli
AU  - Chouchakova N
FAU - Skokowa, Julia
AU  - Skokowa J
FAU - Loscher, Fabian
AU  - Loscher F
FAU - Schmidt, Reinhold E
AU  - Schmidt RE
FAU - Heeringa, Peter
AU  - Heeringa P
FAU - Gessner, J Engelbert
AU  - Gessner JE
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20020430
PL  - United States
TA  - J Biol Chem
JT  - The Journal of biological chemistry
JID - 2985121R
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, IgG)
RN  - 63231-63-0 (RNA)
RN  - EC 3.1.- (Ribonucleases)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/metabolism
MH  - Biotinylation
MH  - Blotting, Southern
MH  - Cells, Cultured
MH  - Chemokine CCL2/metabolism
MH  - Down-Regulation
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Flow Cytometry
MH  - *Gene Expression Regulation
MH  - Glomerular Mesangium/*immunology/metabolism
MH  - Immunohistochemistry
MH  - Kidney/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nephritis/metabolism
MH  - Neutrophils
MH  - RNA/metabolism
MH  - RNA, Messenger/metabolism
MH  - Receptors, IgG/*chemistry
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Ribonucleases/metabolism
EDAT- 2002/05/02 10:00
MHDA- 2002/08/23 10:01
CRDT- 2002/05/02 10:00
PHST- 2002/05/02 10:00 [pubmed]
PHST- 2002/08/23 10:01 [medline]
PHST- 2002/05/02 10:00 [entrez]
AID - S0021-9258(18)60106-1 [pii]
AID - 10.1074/jbc.M200419200 [doi]
PST - ppublish
SO  - J Biol Chem. 2002 Jul 26;277(30):27535-44. doi: 10.1074/jbc.M200419200. Epub 2002 
      Apr 30.