one another, resulting in the anomalous biochemi- 
cal properties of the variant molecule. 
III. Enterotoxin-mediated T Cell Activation. 
Studies of the mechanisms of human T cell ac- 
tivation led to the observation that the in vitro 
proliferative response of purified T cells to Staphy- 
lococcus enterotoxin A (SEA) w^as dependent on 
the presence of HLA class Il-bearing cells in the 
culture system. Class Il-positive accessory cells 
(Raji and HLA-DR, -DQ, or -DP-transfected mouse 
fibroblasts) supported proliferative responses of T 
cells to SEA, w^hile class Il-negative versions of 
these cells did not. Unlike conventional antigens, 
the response to SEA was not restricted by the re- 
sponder haplotype. These data suggested a novel 
interaction of SEA v^ith class II molecules in forma- 
tion of a mitogenic complex. This hypothesis w^as 
confirmed by demonstration that fluorescein-conju- 
gated SEA bound to HLA class Il-transfected mouse 
fibroblasts but not to untransfected cells. More- 
over, by direct immunoprecipitation w^ith SEA- 
PUBLICATIONS 
Sepharose, bands were precipitated from Raji cells 
and class II transfectants that comigrated with the 
class II A and B chains precipitated with the class 
Il-specific monoclonal antibody L243. In contrast, 
SEA-Sepharose did not precipitate any proteins 
fi-om class Il-negative cells. Such data led to the 
conclusions that SEA is an MHC-class II binding 
protein, that this binding is specific and of relatively 
high avidity, and that it is central to the activity of 
SEA as a T cell mitogen. Together with similar stud- 
ies from other laboratories, as well as recent data 
indicating that the enterotoxins specifically stimu- 
late T cell receptors bearing particular vp seg- 
ments, these findings have provided insights into 
the extraordinary nature of this class of molecules 
and their possible involvement in bacterial host de- 
fenses and the pathogenesis of enterotoxin-medi- 
ated diseases. 
Dr. Rich is also Professor of Microbiology and Im- 
munology and of Medicine at Baylor College of 
Medicine and Attending Physician at its affiliated 
hospitals. 
Articles 
Aldrich, C.J., Rodgers, J.R., and Rich, R.R. 1988. Regulation of Qa-1 expression and determinant modification 
by an //-2Z)-linked gene, Qdm. Immunogenetics 28:334-344. 
ElMasry M.N., and Rich, R.R. 1989. Prostaglandin E2 selectively increases interferon gamma receptor expres- 
sion on human CD8"'" lymphocytes. / Clin Invest 83:1436-1440. 
Han, A.C., Rodgers, J.R., and Rich, R.R. 1988. An unexpectedly labile mitochondrially encoded protein is re- 
quired for Mta expression. Immunogenetics 29:258-264. 
Mollick, J.A., Cook, R.G. , and Rich, R.R . 1989. Class II MHC molecules are specific receptors for Staphylococ- 
cus enterotoxin A. Science 244:817-820. 
Rich, R.R., ElMasry, M.N., and Eox, E.J. 1988. Induction of suppressor T cells by cytokines. Transplant Proc 
20:1156-1157. 
Rodgers, J.R., Aldrich, C.J., and Rich, R.R . 1988. A new MHC locus, Qdm, that modifies expression of Qa-1 de- 
terminants in trans. Mouse News Lett 82:8. 
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