SIGNALING THROUGH NK1.1 TRIGGERS NK CELLS TO DIE BUT INDUCES NK T-CELLS TO PRODUCE INTERLEUKIN-4

Citation
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
Citations number
56
Categorie Soggetti
Immunology
Journal title
ISSN journal
00192805
Volume
93
Issue
2
Year of publication
1998
Pages
296 - 305
Database
ISI
SICI code
0019-2805(1998)93:2<296:STNTNC>2.0.ZU;2-D
Abstract
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.