PMID- 11555580
OWN - NLM
STAT- MEDLINE
DCOM- 20011004
LR  - 20171116
IS  - 1078-0432 (Print)
IS  - 1078-0432 (Linking)
VI  - 7
IP  - 9
DP  - 2001 Sep
TI  - Fas ligand expression by neoplastic T lymphocytes mediates elimination of CD8+ 
      cytotoxic T lymphocytes in mycosis fungoides: a potential mechanism of tumor 
      immune escape?
PG  - 2682-92
AB  - Mycosis fungoides (MF) is the most common form of cutaneous T-cell lymphoma 
      (CTCL) and arises from the accumulation and clonal proliferation of 
      epidermotropic, CD4+/CD45RO+ (helper/memory) T lymphocytes. Loss of CD8+ CTLs 
      within MF lesions is associated with poor prognosis and disease progression. 
      Because T-lymphocyte apoptosis is controlled mainly through the Fas/Fas ligand 
      (FasL) pathway and tumor cells may escape immune surveillance by expressing FasL, 
      triggering apoptosis of tumor-infiltrating T lymphocytes, we studied the role of 
      this system in MF. T-cell subsets, Fas/FasL expression, and apoptosis were 
      evaluated in normal and lesional skin biopsy specimens from 21 patients with all 
      stages of MF and in cultured CTCL cell lines (MJ, HUT78, and HH) using 
      immunohistochemistry, terminal deoxynucleotidyl transferase-mediated dUTP nick 
      end labeling (TUNEL), and Western blotting. MF lesions and paired, clinically 
      "normal," uninvolved skin showed increased numbers of both TUNEL-positive 
      epidermal keratinocytes (n = 13; F = 31.146; P < 0.01, ANOVA) and dermal 
      lymphocyte infiltrates (n = 13; F = 15.825, P < 0.01, ANOVA) compared with the 
      normal control skin. FasL expression was highest in lesional epidermal 
      keratinocytes, in CTCL tumor cell lines, and in dermal tumor lymphocytes in MF 
      lesions compared with uninvolved skin. FasL colocalized with CD45RO+ cells. CD8+ 
      cells in or adjacent to CD45RO+ cells were positively labeled by TUNEL for 
      apoptosis. In addition, CD8+ cell numbers were decreased in areas in which FasL+ 
      tumor cells were abundant (2.01 +/- 0.86%) compared with non-FasL expressing 
      areas (13.53 +/- 3.54%; P < 0.02). These results suggest that a potential 
      mechanism of tumor immune escape in MF is FasL-mediated apoptosis of infiltrating 
      CD8+ CTLs.
FAU - Ni, X
AU  - Ni X
AD  - Department of Dermatology, University of Texas, M. D. Anderson Cancer Center, 
      Houston, Texas 77030, USA.
FAU - Hazarika, P
AU  - Hazarika P
FAU - Zhang, C
AU  - Zhang C
FAU - Talpur, R
AU  - Talpur R
FAU - Duvic, M
AU  - Duvic M
LA  - eng
GR  - CA 16672-22/CA/NCI NIH HHS/United States
GR  - R21-CA74117/CA/NCI 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  - Clin Cancer Res
JT  - Clinical cancer research : an official journal of the American Association for 
      Cancer Research
JID - 9502500
RN  - 0 (CD8 Antigens)
RN  - 0 (FASLG protein, human)
RN  - 0 (Fas Ligand Protein)
RN  - 0 (Membrane Glycoproteins)
RN  - EC 3.1.3.48 (Leukocyte Common Antigens)
SB  - IM
MH  - Adult
MH  - Aged
MH  - Apoptosis
MH  - CD8 Antigens/*metabolism
MH  - Fas Ligand Protein
MH  - Female
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Nick-End Labeling
MH  - Jurkat Cells
MH  - Leukocyte Common Antigens/metabolism
MH  - Male
MH  - Membrane Glycoproteins/*biosynthesis
MH  - Middle Aged
MH  - Mycosis Fungoides/immunology/metabolism/*pathology
MH  - Skin/chemistry/immunology/pathology
MH  - Skin Neoplasms/immunology/metabolism/*pathology
MH  - T-Lymphocytes/chemistry/*immunology/pathology
MH  - T-Lymphocytes, Cytotoxic/*immunology/metabolism/pathology
MH  - Tumor Cells, Cultured
EDAT- 2001/09/14 10:00
MHDA- 2001/10/05 10:01
CRDT- 2001/09/14 10:00
PHST- 2001/09/14 10:00 [pubmed]
PHST- 2001/10/05 10:01 [medline]
PHST- 2001/09/14 10:00 [entrez]
PST - ppublish
SO  - Clin Cancer Res. 2001 Sep;7(9):2682-92.