The immunopathology of intraocular tumour rejection was studied using two transplantable tumours in mice. UV5C25 fibrosarcoma and P91 mastocytoma express tumour specific antigens that elicit strong systemic T cell-mediated immune responses following intracameral transplantation. Although both tumours underwent immunological rejection, the immunopathological sequelae of tumour rejection differed markedly. P91 tumour rejection was accompanied by bulk ischaemic necrosis, microvascular damage, and extensive damage to innocent bystander cells. A large body of experimental evidence indicated that this ischaemic necrotic pattern of intraocular tumour rejection was the result of a delayed-type hypersensitivity (DTH) effector mechanism. By contrast, intraocular UV5C25 tumour rejection occurred by piecemeal necrosis and did not culminate in injury to juxtaposed normal host tissues. The results of in vitro and in vivo experiments strongly indicated a role for cytotoxic T lymphocyte (CTL) mediated mechanisms in the piecemeal necrotic pattern of tumour rejection. Collectively, the results indicated that although tumour bearing hosts possessed both CTL and DTH effector mechanisms, only one form of T cell-mediated immunity prevailed within the intraocular milieu.
- Cytotoxict lymphocytes
- Delayed type hypersensitivity
- T cell
ASJC Scopus subject areas
- Sensory Systems