PMID- 9800958
OWN - NLM
STAT- MEDLINE
DCOM- 19981116
LR  - 20171116
IS  - 0023-6837 (Print)
IS  - 0023-6837 (Linking)
VI  - 78
IP  - 10
DP  - 1998 Oct
TI  - Control of monocyte influx in glomerulonephritis in transplanted kidneys in the 
      rat.
PG  - 1327-37
AB  - Induction of anti-Thy-1 nephritis in different strains of inbred rats results in 
      phenotypically different types of renal diseases. In Wistar and Lewis (LEW) rats, 
      a transient influx of ED1+ macrophages occurs 24 hours after injection of 
      anti-Thy-1 antibodies, whereas this does not occur in F344 rats. The present 
      experiments were designed to investigate the role of the kidney in the regulation 
      of the monocyte influx in this model. To dissociate the role of the immune system 
      from local intrarenal factors in the control of monocyte influx, anti-Thy-1 
      nephritis was induced in LEW rats with an F344 kidney transplant and in F344 rats 
      with a LEW kidney allograft. Acute rejection episodes were prevented by treatment 
      with an anti-CD4 monoclonal antibody. Control rats received a syngeneic kidney 
      graft. Monocyte influx after injection of anti-Thy-1 antibodies was found in the 
      glomeruli of both LEW and F344 kidneys removed from LEW recipients, whereas there 
      was no demonstrable monocyte influx after infusion of anti-Thy-1 antibodies in 
      either LEW or F344 kidneys removed from F344 recipients. Monocyte infiltration 
      correlated with the subsequent expansion of the mesangial extracellular matrix. 
      The inability to attract monocytes was not due to the lack of glomerular 
      expression of chemokines, because F344 and LEW glomeruli demonstrated a similar 
      expression of monocyte chemoattractant protein-1 (MCP-1). Differences in the 
      ability to activate the complement system were excluded. We conclude that the 
      immune system controls the glomerular influx of monocytes and that the reaction 
      of the mesangial cells is probably controlled by combinations of cytokines 
      produced during the inflammatory process.
FAU - De Heer, E
AU  - De Heer E
AD  - Department of Pathology, Leiden University Medical Center, The Netherlands.
FAU - Prodjosudjadi, W
AU  - Prodjosudjadi W
FAU - Davidoff, A
AU  - Davidoff A
FAU - van der Wal, A
AU  - van der Wal A
FAU - Bruijn, J A
AU  - Bruijn JA
FAU - Paul, L C
AU  - Paul LC
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Lab Invest
JT  - Laboratory investigation; a journal of technical methods and pathology
JID - 0376617
RN  - 0 (Antigens, CD34)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Proliferating Cell Nuclear Antigen)
RN  - 0 (Thy-1 Antigens)
SB  - IM
MH  - Animals
MH  - Antigens, CD34/analysis
MH  - Chemokine CCL2/analysis
MH  - Extracellular Matrix/pathology
MH  - Glomerular Mesangium/pathology
MH  - Glomerulonephritis/*pathology
MH  - Kidney Transplantation/*pathology/physiology
MH  - Macrophages/pathology
MH  - Male
MH  - Monocytes/*pathology/physiology
MH  - Proliferating Cell Nuclear Antigen/analysis
MH  - Rats
MH  - Rats, Inbred F344
MH  - Rats, Inbred Lew
MH  - Rats, Wistar
MH  - Thy-1 Antigens/immunology
MH  - Transplantation, Homologous/pathology
MH  - Transplantation, Isogeneic/pathology
EDAT- 1998/11/04 00:00
MHDA- 1998/11/04 00:01
CRDT- 1998/11/04 00:00
PHST- 1998/11/04 00:00 [pubmed]
PHST- 1998/11/04 00:01 [medline]
PHST- 1998/11/04 00:00 [entrez]
PST - ppublish
SO  - Lab Invest. 1998 Oct;78(10):1327-37.