Open AccessDecreased expression of 20‐kD homologous restriction factor (HRF20, CD59) on T lymphocytes in Epstein–Barr virus (EBV)‐induced infectious mononucleosis
Author(s) -
KAWANO M.,
TSUNODA S.,
KONI I.,
MABUCHI H.,
MURAMOTO H.,
YACHIE A.,
SEKI H.
Publication year - 1997
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1046/j.1365-2249.1997.d01-999.x
Subject(s) - mononucleosis , immunology , virology , epstein–barr virus , virus , homologous chromosome , biology , cd59 , epstein–barr virus infection , antibody , complement system , genetics , gene
HRF20 (CD59) is one of the membrane‐associated complement regulatory proteins. The characteristic function of CD59 is to prevent membrane attack complex (MAC) formation on the cell surface and to protect the cell from complement‐mediated cell lysis. We examined the expression of CD59 antigen on T cell subpopulations in patients with acute infectious mononucleosis (IM) and analysed the relationship between the amount of CD59 expression and activation‐induced cell death of mature T cells with apoptosis. Decreased expression of CD59 on CD8 + T cells, especially on CD45RO + and HLA‐DR + activated T cells, was marked in acute IM patients. In contrast, activated CD4 + T cells from IM patients expressed as much CD59 antigen as CD4 + T cells from healthy volunteers. After incubation‐induced cell death, viable CD8 + T cells showed normal amounts of CD59 antigen on their surface. CD59 dim CD8 + T cells were more susceptible to apoptosis than CD59 bright CD8 + T cells. These findings suggest that decreased expression of CD59 on CD8 + T cells may discriminate the susceptibility of activated CD8 + T cells to activation‐induced cell death in IM.