PMID- 9491917
OWN - NLM
STAT- MEDLINE
DCOM- 19980402
LR  - 20171116
IS  - 0889-2229 (Print)
IS  - 0889-2229 (Linking)
VI  - 14
IP  - 3
DP  - 1998 Feb 10
TI  - Expression of FAP-1 (Fas-associated phosphatase) and resistance to Fas-mediated 
      apoptosis in T cell lines derived from human T cell leukemia virus type 
      1-associated myelopathy/tropical spastic paraparesis patients.
PG  - 261-7
AB  - Human T cell leukemia virus type 1 (HTLV-I) is the etiologic agent of 
      HTLV-I-associated myelopathy/tropical spastic paraparesis (HAM/TSP) with an 
      autoimmune condition. We examined the sensitivity of HTLV-I-infected T cell lines 
      to Fas-mediated apoptosis, which plays a critical role in the elimination of 
      self-reactive T cells. Among 13 human T-cell lines, all 4 HAM-derived T cell 
      lines and 4 of 6 non-HAM/HTLV-I T cell lines were resistant to apoptosis induced 
      by anti-Fas antibody, whereas only 1 of 3 uninfected cell lines was resistant to 
      apoptosis. The cell lines resistant to apoptosis expressed the viral tax gene 
      and/or the cellular FAP-1 (Fas-associated phosphatase) gene, both of which 
      inhibit Fas-mediated apoptosis in T cell lines. Although Tax is a transcriptional 
      activator of a number of cellular genes, the expression of Tax in a T cell line 
      did not induce the expression of FAP-1, suggesting that these two antiapoptotic 
      proteins independently function in HTLV-I-infected cells. Seven of 10 
      HTLV-I-infected cell lines, compared with only 1 of 3 virus-negative cell lines, 
      expressed FAP-1. All four HAM cell lines expressed the FAP-1 gene, and its level 
      in these cells was higher than in other T cell lines. Our results suggest that 
      virus-infected T cells escape Fas-mediated immune surveillance by the function of 
      Tax and FAP-1, and this escape may be involved in the autoimmune condition 
      observed in HAM/TSP patients.
FAU - Arai, M
AU  - Arai M
AD  - Department of Immunotherapeutics, Medical Research Division, Tokyo Medical and 
      Dental University, Yushima, Japan.
FAU - Kannagi, M
AU  - Kannagi M
FAU - Matsuoka, M
AU  - Matsuoka M
FAU - Sato, T
AU  - Sato T
FAU - Yamamoto, N
AU  - Yamamoto N
FAU - Fujii, M
AU  - Fujii M
LA  - eng
GR  - R0I-GM55417/GM/NIGMS 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  - United States
TA  - AIDS Res Hum Retroviruses
JT  - AIDS research and human retroviruses
JID - 8709376
RN  - 0 (Carrier Proteins)
RN  - 0 (Gene Products, tax)
RN  - 0 (fas Receptor)
RN  - 6PLQ3CP4P3 (Etoposide)
RN  - 80168379AG (Doxorubicin)
RN  - EC 3.1.3.48 (PTPN13 protein, human)
RN  - EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 1)
RN  - EC 3.1.3.48 (Protein Tyrosine Phosphatase, Non-Receptor Type 13)
RN  - EC 3.1.3.48 (Protein Tyrosine Phosphatases)
SB  - IM
MH  - *Apoptosis
MH  - Blotting, Northern
MH  - Carrier Proteins/genetics/*physiology
MH  - Cell Line, Transformed
MH  - Doxorubicin/pharmacology
MH  - Etoposide/pharmacology
MH  - Flow Cytometry
MH  - Gene Expression
MH  - Gene Products, tax/genetics/physiology
MH  - Human T-lymphotropic virus 1/*physiology
MH  - Humans
MH  - Paraparesis, Tropical Spastic/*immunology
MH  - Protein Tyrosine Phosphatase, Non-Receptor Type 1
MH  - Protein Tyrosine Phosphatase, Non-Receptor Type 13
MH  - Protein Tyrosine Phosphatases/genetics/*physiology
MH  - T-Lymphocytes/*cytology/drug effects/enzymology/*virology
MH  - fas Receptor/physiology
EDAT- 1998/03/10 00:00
MHDA- 1998/03/10 00:01
CRDT- 1998/03/10 00:00
PHST- 1998/03/10 00:00 [pubmed]
PHST- 1998/03/10 00:01 [medline]
PHST- 1998/03/10 00:00 [entrez]
AID - 10.1089/aid.1998.14.261 [doi]
PST - ppublish
SO  - AIDS Res Hum Retroviruses. 1998 Feb 10;14(3):261-7. doi: 10.1089/aid.1998.14.261.