Several superantigens stimulate both CD4 and CD8 T
cells, such as streptococcal pyrogenic exotoxins A and B,
and Mycoplasma arthritidis mitogen. The CD8 T cell response
to staphylococcal enterotoxins was reviewed by Herrmann and
MacDonald in Seminars in Immunology, 5:33 (1993). They
raised the possibility that the proliferation of CD8 T cells
was due to the high lymphokine titers achieved by the
stimulation of the co-cultivated CD8 T cells, so they
apparently did not stimulate purified CD8 T cells. Probably
the stimulation cannot be done without CD4 cells, because of
the requirement for IL-2. I don't know what is going on
mechanistically, but Herrmann and coworkers found that the
activation of CD8 T cells by staphylococcal enterotoxins is
independent of the CD8 molecule, and Labrecque suggested
that class I-restricted TCR's have a low intrinsic affinity
for MHC class II molecules.
The requirement for MHC class II probably depends on
the assay and the superantigen. SEC1 binds poorly to murine
class II antigens. Avery et al. (J. Immunol. 153:4853
(1994) found that lymph node cells from class II-deficient
mice responded strongly to SEC-1, SEC-2, SEC-3, and SEE, but
not to SEA, SEB, or SED.
Jack Komisar
