PMID- 11261791
OWN - NLM
STAT- MEDLINE
DCOM- 20010329
LR  - 20071114
IS  - 0741-5400 (Print)
IS  - 0741-5400 (Linking)
VI  - 69
IP  - 3
DP  - 2001 Mar
TI  - Lymphocytes induce monocyte chemoattractant protein-1 production by renal cells 
      after Fc gamma receptor cross-linking: role of IL-1beta.
PG  - 435-9
AB  - Leukocyte recruitment to the kidney in immune complex disease like systemic lupus 
      erythematosus (SLE) is mediated in part by local expression of chemokines such as 
      monocyte chemoattractant protein-1 (MCP-1). Recent studies from this laboratory 
      demonstrated that cross-linking Fc gammaR on lymphocytes causes release of a 
      soluble factor that induces monocyte chemokine production. To explain the 
      induction of renal chemokine expression in immune complex disease, we postulated 
      that this lymphocyte factor stimulates renal parenchymal cell MCP-1 expression. 
      To test this hypothesis, human peripheral blood lymphocytes were incubated on 
      immobilized IgG, a model for immune complex Fc gammaR cross-linking. Supernatants 
      from these lymphocyte cultures significantly increased MCP-1 production by human 
      mesangial, glomerular capillary endothelial, and proximal tubular epithelial 
      cells. Mesangial cells incubated on immobilized IgG or with soluble, preformed 
      immune complexes did not secrete MCP-1 above control levels. Lymphocyte 
      supernatant-induced MCP-1 production appeared to be dependent on the presence of 
      interleukin (IL)-1beta in the supernatant. Removing IL-1beta from the 
      supernatants, antagonizing its activity, or preventing conversion to mature 
      IL-1beta abrogated renal cell MCP-1 expression by the lymphocyte supernatants. 
      These data demonstrate that in response to cross-linking Fc gammaR, lymphocytes 
      induce renal cell MCP-1 expression by secreting IL-1beta. Renal chemokine 
      expression in immune complex disease may thus be triggered as lymphocytes traffic 
      through the kidney and encounter deposited immune complexes.
FAU - Rovin, B H
AU  - Rovin BH
AD  - Department of Internal Medicine and the Heart Lung Research Institute, The Ohio 
      State University School of Medicine and Public Health, USA. rovin.1@osu.edu
FAU - Lu, L
AU  - Lu L
FAU - Marsh, C B
AU  - Marsh CB
LA  - eng
GR  - DK46055/DK/NIDDK NIH HHS/United States
GR  - HL63800/HL/NHLBI NIH HHS/United States
GR  - RR00034/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
RN  - 0 (Antigen-Antibody Complex)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Interleukin-1)
RN  - 0 (Receptors, IgG)
SB  - IM
MH  - Antigen-Antibody Complex/immunology/metabolism
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis
MH  - Humans
MH  - Immunoglobulin G/immunology/pharmacology
MH  - Interleukin-1/antagonists & inhibitors/*physiology
MH  - Kidney/cytology/immunology/*metabolism
MH  - Lymphocyte Activation/immunology
MH  - Lymphocytes/*immunology/metabolism
MH  - Receptors, IgG/immunology/*metabolism
EDAT- 2001/03/23 10:00
MHDA- 2001/04/03 10:01
CRDT- 2001/03/23 10:00
PHST- 2001/03/23 10:00 [pubmed]
PHST- 2001/04/03 10:01 [medline]
PHST- 2001/03/23 10:00 [entrez]
PST - ppublish
SO  - J Leukoc Biol. 2001 Mar;69(3):435-9.