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The LFA‐3 Adhesion Pathway is Differently Utilized by Superantigen‐Activated Human CD4 + T‐Cell Subsets
Author(s) -
GJÖRLOFF A.,
HEDLUND G.,
KALLAND T.,
SANSOM D.,
FISCHER H.,
TROWSDALE J.,
SJÖGREN H. O.,
DOHLSTEN M.
Publication year - 1992
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1992.tb03096.x
Subject(s) - superantigen , microbiology and biotechnology , cell adhesion , adhesion , t cell , immunology , cell , biology , chemistry , genetics , immune system , organic chemistry
The superantigen SFA binds to MHC class II molecules and activates a large fraction off cells as a result of iteraction with particular TCR‐Vβ 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 a (HLA‐DR4/LFA‐3 double transfectants) supported a vigorous T‐cell proliferation and required 1000‐fold lower SEA concentration than DR4‐transfected eells. DR4/LFA‐3 double transfectants presenting SEA to CD4 + T cells induced large amounts of IFN‐γ, while single DR4 transfectants failed to elicit IFN‐γ 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‐γ 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 lo the aecessory DR4/LFA‐3 cells. Human CD4 + T‐cell lines medialed a low level of SFA‐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 thai Ihe CD4 + naive and memory T‐helper cells are different in their response to LFA‐3 as an accessory molecule.