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Immunological unresponsiveness and apoptotic cell death of T cells in measles virus infection
Author(s) -
ADDAE MICHAEL MARK,
KOMADA YOSHIHIRO,
ZHANG XAOLI,
SAKURAI MINORU
Publication year - 1995
Publication title -
pediatrics international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.49
H-Index - 63
eISSN - 1442-200X
pISSN - 1328-8067
DOI - 10.1111/j.1442-200x.1995.tb03320.x
Subject(s) - il 2 receptor , measles virus , cd8 , programmed cell death , t cell , interleukin 21 , cytotoxic t cell , apoptosis , antigen , medicine , cd3 , immunology , zap70 , biology , virology , immune system , measles , in vitro , vaccination , biochemistry
The phenotypic alterations associated with T cells during measles virus infection have been demonstrated and an attempt has been made to show programmed cell death (PCD) of T cells activated in vivo. During the acute phase of illness, activated T cells increased rapidly. Memory T cells (CD45RO + ), especially CD8 + memory T cells also tend to increase. During the recovery phase, CD8 + T cells declined rapidly, and naive (CD45RA + ) T cells increased in numbers. The anti‐CD3 monoclonal antibody‐induced expression of interleukin‐2 receptor (CD25) was suppressed. However, the addition of phorbol 12‐myristate 13‐acetate (PMA) caused the significant recovery of CD25 expression. In addition, PCD of activated T cells from measles patients was induced in culture. After triggering of the T cell receptor‐CD3 complex, cells became more susceptible to PCD. Interestingly, the addition of PMA could inhibit PCD of activated T cells. Taken together, these data suggest unresponsiveness and activation‐induced cell death of T cells during the primary response to measles virus antigens, depending on the activation status of protein kinase C.