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CD95 (Fas) ligand expression of Epstein‐Barr virus (EBV)‐infected lymphocytes: A possible mechanism of immune evasion in chronic active EBV infection
Author(s) -
Ohshima Koichi,
Suzumiya Junji,
Sugihara Midori,
Nagafuchi Seiho,
Ohga Shouichi,
Kikuchi Masahiro
Publication year - 1999
Publication title -
pathology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.73
H-Index - 74
eISSN - 1440-1827
pISSN - 1320-5463
DOI - 10.1046/j.1440-1827.1999.00816.x
Subject(s) - fas ligand , perforin , ctl* , granzyme , immunology , cytotoxic t cell , biology , fas receptor , granzyme b , cd8 , immune system , epstein–barr virus , virology , virus , apoptosis , programmed cell death , biochemistry , in vitro
The Epstein‐Barr virus (EBV) induces infectious mononucleosis (IM) and can be associated with chronic active EBV infection (CAEBV). Cytotoxic T lymphocytes (CTL) play an important role in excluding EBV‐infected cells. Two cytotoxic mechanisms of CTL have been demonstrated: one perforin/granzyme‐based and the other Fas (CD95)/Fas ligand (FasL)‐based. To clarify these two pathways in CAEBV, we analyzed six patients with CAEBV and four patients with IM using immunohistochemical staining of the lymph nodes. In both CAEBV and IM, CD8 + T‐cells increased in number, but CD56 + natural killer cells were rare. In four of six cases with CAEBV, approximately half the lymphocytes were positive for T cell‐restricted intracellular antigens (TIA‐1), which were recognized by the cytolytic granules of CTL. In IM, the number of TIA‐1 positive cells was smaller than that in CAEBV. Fas‐positive lymphocytes were frequently encountered in both CAEBV and IM. However, FasL‐positive lymphocytes increased in three of six patients with CAEBV, but not in patients with IM. Except for one case with CAEBV, the number of perforin‐ and/or granzyme‐positive cells was small in number in both CAEBV and IM cases. In double‐staining FasL and EBV in situ hybridization, FasL‐positive EBV‐infected lymphocytes were detected in CAEBV but not in IM. In CAEBV, the Fas/FasL pathway and not perforin pathways appears to play an important role in the pathogenesis. The data suggest that EBV‐infected lymphocytes may evade immune attack through the expression of FasL.