PMID- 8882134
OWN - NLM
STAT- MEDLINE
DCOM- 19961216
LR  - 20190503
IS  - 0003-4967 (Print)
IS  - 1468-2060 (Electronic)
IS  - 0003-4967 (Linking)
VI  - 55
IP  - 9
DP  - 1996 Sep
TI  - Cytokine production by endothelial cells infected with human T cell lymphotropic 
      virus type I.
PG  - 632-7
AB  - OBJECTIVE: To investigate the ability of human T cell lymphotropic virus type I 
      (HTLV-I) to infect endothelial cells and induce cytokine production by these 
      cells. METHODS: Human umbilical vein endothelial cells (HUVEC) were cocultured 
      with HTLV-I infected T cell line (MT-2 cells) or uninfected T cell line (CEM 
      cells). RESULTS: Following coculture with MT-2 cells, endothelial cells expressed 
      HTLV-I specific core antigens. Endothelial cells cocultured with MT-2 cells 
      produced significant amounts of several cytokines, including interleukin (IL)-1 
      alpha, IL-6, granulocyte colony stimulating factor (G-CSF), and 
      granulocyte/macrophage colony stimulating factor (GM-CSF), compared with 
      endothelial cells cocultured with CEM cells. Coculturing of endothelial cells 
      with MT-2 and CEM cells failed to produce detectable amounts of IL-1 beta and 
      tumour necrosis factor alpha (TNF-alpha). The production of cytokines by 
      endothelial cells cocultured with MT-2 cells was more persistent than that by 
      endothelial cells cocultured with CEM cells after several passages. Furthermore, 
      the production was blocked by cocultivation of endothelial cells and MT-2 cells 
      using the Millicell system. Finally, after cocultivation of endothelial cells and 
      MT-2 cells, endothelial cells positive for HTLV-I antigen were stained by 
      anti-GM-CSF antibody. CONCLUSIONS: HTLV-I can infect endothelial cells, resulting 
      in their active production of several cytokines, such as IL-1 alpha, IL-6, G-CSF, 
      and GM-CSF. These findings strongly suggest that the excess production of these 
      cytokines by HTLV-I infected endothelial cells may be involved in the 
      pathogenesis of HTLV-I associated inflammatory diseases.
FAU - Takashima, H
AU  - Takashima H
AD  - First Department of Internal Medicine, Nagasaki University, Japan.
FAU - Eguchi, K
AU  - Eguchi K
FAU - Kawakami, A
AU  - Kawakami A
FAU - Kawabe, Y
AU  - Kawabe Y
FAU - Migita, K
AU  - Migita K
FAU - Sakai, M
AU  - Sakai M
FAU - Origuchi, T
AU  - Origuchi T
FAU - Nagataki, S
AU  - Nagataki S
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Ann Rheum Dis
JT  - Annals of the rheumatic diseases
JID - 0372355
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 143011-72-7 (Granulocyte Colony-Stimulating Factor)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
SB  - IM
MH  - Cell Line
MH  - Coculture Techniques
MH  - Cytokines/*metabolism
MH  - Deltaretrovirus Infections/*immunology
MH  - Endothelium, Vascular/metabolism/*virology
MH  - Granulocyte Colony-Stimulating Factor/metabolism
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/metabolism
MH  - Humans
MH  - Immunohistochemistry
MH  - Interleukin-1/metabolism
MH  - Interleukin-6/metabolism
MH  - T-Lymphocytes/immunology
PMC - PMC1010260
EDAT- 1996/09/01 00:00
MHDA- 1996/09/01 00:01
PMCR- 1999/09/01
CRDT- 1996/09/01 00:00
PHST- 1996/09/01 00:00 [pubmed]
PHST- 1996/09/01 00:01 [medline]
PHST- 1996/09/01 00:00 [entrez]
PHST- 1999/09/01 00:00 [pmc-release]
AID - 10.1136/ard.55.9.632 [doi]
PST - ppublish
SO  - Ann Rheum Dis. 1996 Sep;55(9):632-7. doi: 10.1136/ard.55.9.632.