Intracameral (IC) inoculation of syngeneic B16F10 melanoma cells into the anterior chamber of C57BL/6 mice evoked specific impairment of delayed-type hypersensitivity (DTH) responses, yet stimulated significant humoral antibody production. However, the presence of anti-melanoma antibodies did not protect against progressive tumor growth. In contrast to the results with intracameral inoculations, subcutaneous injection of B16F10 melanoma cells induced significant DTH responsiveness in C57BL/6 hosts. Adoptive transfer experiments showed that T-suppressor cells, induced by IC inoculation of viable syngeneic melanoma cells, inhibited specifically the development of DTH responses to melanoma-associated antigens (MAA). The IC-induced T-suppressor cell population was found to be cyclophosphamide-sensitive and antigen-specific, suggesting that possibly a first-order suppressor pathway had been activated. IC inoculation of nonproliferating (i.e, X-irradiated) melanoma cells evoked a similar inhibition of specific DTH responses, and stimulated similar levels of serum antibodies, yet induced a solid state of immunity to subsequent tumor challenge. The IC-induced immunity was (1) DTH-independent; (2) specific for B16F10 melanoma - third party tumors were not rejected; and (3) presumably not mediated directly by antibodies. Thus, IC presentation of nonproliferating melanoma cells evokes an aberrant immune response in which DTH responses are profoundly suppressed, yet the host is immune to secondary tumor challenge.
|Original language||English (US)|
|Number of pages||8|
|Journal||Investigative Ophthalmology and Visual Science|
|State||Published - 1984|
ASJC Scopus subject areas
- Sensory Systems
- Cellular and Molecular Neuroscience