A. Asea et J. Steinstreilein, SIGNALING THROUGH NK1.1 TRIGGERS NK CELLS TO DIE BUT INDUCES NK T-CELLS TO PRODUCE INTERLEUKIN-4, Immunology, 93(2), 1998, pp. 296-305
In vivo inoculation of specific antibody is an accepted protocol for e
limination of specific cell populations. Except for anti-CD3 and anti-
CD4, it is not known if the depleted cells are eliminated by signallin
g through the target molecule or through a more non-specific mechanism
. C57BL/6 mice were inoculated with anti-natural killer (NK1.1) monocl
onal antibody (mAb). Thereafter spleen cells were harvested, stained f
or both surface and intracellular markers, and analysed by flow cytome
try. As early as 2 hr post inoculation, NK cells were signalled to bec
ome apoptotic while signalling through the NK1.1 molecule activated NK
1.1(+) T-cell receptor (TCR)(+) (NK T) sells to increase in number: an
d produce interleukin-4 (IL-4). Anti NK1.1 mAb was less efficient at s
ignalling apoptosis in NK cells when NK T-cell deficient [beta 2-micro
globulin beta 2m-deficient] mice were used compared with wild type mic
e. Efficient apoptotic signalling was restored when beta 2m-deficient
mice were reconstituted with NK T cells. NK-specific antibody best sig
nals the apoptotic process in susceptible NK cells when resistant NK T
cells are present, activated, and secrete IL-4.