Tumour cells transfected with cDNAs encoding non-self proteins were used to
investigate the ability of the immune system to respond to immunogenic ant
igens expressed by tumours. Secreted, intracellular and surface proteins we
re used as model antigens, as these reflect the potential forms of tumour a
ntigens. Syngeneic BALB/c mice injected with viable line 1 lung carcinoma o
r EMT6 mammary tumour cells secreting ovalbumin (OVA) or prostate-specific
antigen (PSA) produced very high immunoglobulin G (IgG) antibody titres, eq
uivalent to those of mice injected with protein in Freund's complete adjuva
nt (FCA). Secretion of the antigens was not necessary as tumour cells expre
ssing a cell-surface antigen (HER-2/Neu) or an intracellular antigen - gree
n fluorescence protein (GFP) - also generated high-titre antigen-specific I
gG antibodies. In interleukin-4 (IL-4)-deficient mice, both IgG1 and IgG2a
were produced in response to OVA administered in FCA, whereas in response t
o tumour-produced antigen, the antibodies switched from predominantly IgG1
to IgG2a, indicating that the mechanisms responsible for antibody induction
different between these forms of immunization. In contrast to the line 1 a
nd EMT6 tumours, which are of BALB/c origin, OVA- or PSA-producing B16 mela
noma cells, which are of C57BL/6 origin failed to elicit antibody productio
n. This was not the result of strain differences, as a similar finding was
observed when the tumours were grown in (BALB/c x C57BL/6)F-1 mice, but app
eared to be caused by intrinsic differences in the tumours. Furthermore, co
-injection of both B16/OVA and line 1 tumours resulted in production of ant
i-OVA antibody, indicating that B16 tumours were not immunosuppressive, but
instead line 1 tumours appear to exert an adjuvant effect.