The existence of a naturally occurring immunosurveillance against neop
lastic cells is controversial, A difficulty with this concept is that
tumor-specific antigen-reactive T cells would not be expected to becom
e activated after encountering tumor cells, since T cells that bind to
antigen in the absence of the costimulation provided by antigen-prese
nting cells may be inactivated, We studied a transgenic model of tumor
igenesis where T cells reactive to a particular tumor-specific antigen
are lost prior to the development of non-antigen-presenting cell-deri
ved tumors; therefore, the tumors that develop are not subjected to im
munosurveillance. We found that a tumor cell line derived from one suc
h tumor expresses the T-cell costimulatory molecule B7-1, the expressi
on of which is normally restricted to antigen-presenting cells, In add
ition, we found that several immortalized cell lines, which are nontum
origenic and thus have suffered only early genetic events in the tumor
igenesis process, express B7. This suggests that a host cell can be in
duced to express surface B7-1 molecules after suffering an oncogenic i
nsult, which might possibly be a primary mechanism of immunosurveillan
ce against tumors.