RETRACTED: A lymphokine that activates the cytolytic program of both cytotoxic T lymphocyte and natural killer clones.
Author(s) -
C Milanese,
Robert F. Siliciano,
Reinhold Schmidt,
Jerome Ritz,
Neil Richardson,
E L Reinherz
Publication year - 1986
Publication title -
the journal of experimental medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 8.483
H-Index - 448
eISSN - 1540-9538
pISSN - 0022-1007
DOI - 10.1084/jem.163.6.1583
Subject(s) - cytotoxic t cell , lymphokine , biology , lytic cycle , major histocompatibility complex , mhc class i , cytolysis , antigen , microbiology and biotechnology , lymphokine activated killer cell , natural killer cell , immunology , effector , interleukin 21 , cd8 , in vitro , biochemistry , virus
A 10-12 kD lymphokine, herein termed TCAF, was recently shown to be secreted from Th after crosslinking of their antigen/MHC (T3-Ti) receptors. TCAF stimulates resting T lymphocyte proliferation via binding to surface components of the T11 pathway. To determine whether TCAF could induce antigen-independent activation of the lytic machinery of cytotoxic cells, the present studies were conducted. In the presence of TCAF, both T8+ class I MHC-specific and T4+ class II MHC-specific cytotoxic T cell clones were induced to kill targets, including those lacking the appropriate MHC molecules. This effect was unique to TCAF, since IL-1, IL-2, IFN-gamma could not stimulate lytic activity. Furthermore, both T3+T11+ and T3-T11+ NK clones were triggered to lyse NK-resistant target cells. These findings suggest that TCAF can function in an antigen-independent fashion to amplify cytotoxic effector responses.
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