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The LFA-3 adhesion pathway is differently utilized by superantigen-activated human CD4+ T-cell subsets.

Abstract：

:The superantigen SEA binds to MHC class II molecules and activates a large fraction of T cells as a result of interaction with particular TCR-V beta sequences. MHC class II transfected CHO cells induce a marginal CD4+ T-cell proliferation in the presence of SEA. CHO cells transfected with both MHC class II and LFA-3 (HLA-DR4/LFA-3 double transfectants) supported a vigorous T-cell proliferation and required 1000-fold lower SEA concentration than DR4-transfected cells. DR4/LFA-3 double transfectants presenting SEA to CD4+ T cells induced large amounts of IFN-gamma, while single DR4 transfectants failed to elicit IFN-gamma production. CD4+45RA+ naive T cells proliferated much more strongly compared with CD4+45R0+ memory T cells when SEA was presented by the DR4/LFA-3-transfected cells. In contrast, IFN-gamma production was only detected in CD4+45R0+ memory cells. The enhanced proliferation by the CD4+45RA+ naive T cells was not due to a stronger binding to the accessory DR4/LFA-3 cells. Human CD4+ T-cell lines mediated a low level of SEA-dependent cell-mediated cytotoxicity (SDCC) against DR4 target cells, whereas a strong SDCC was mediated against DR4/LFA-3-expressing target cells. These results demonstrate that superantigen-activated human CD4+ T cells require the adhesion molecule LFA-3 for optimal stimulation and that the CD4+ naive and memory T-helper cells are different in their response to LFA-3 as an accessory molecule.

journal_name

Scand J Immunol

journal_title

Scandinavian journal of immunology

authors

Gjörloff A,Hedlund G,Kalland T,Sansom D,Fischer H,Trowsdale J,Sjögren HO,Dohlsten M

doi

10.1111/j.1365-3083.1992.tb03096.x

keywords:

subject

Has Abstract

pub_date

1992-08-01 00:00:00

pages

243-50

issue

2

eissn

0300-9475

issn

1365-3083

journal_volume

36

pub_type

杂志文章

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