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Abstract
The authors have studied histopathologically the growth, invasion, and regression of allogeneic P815 mastocytoma cells placed in the anterior chambers of eyes of three different strains of inbred mice. Previous clinical observations had suggested that the degree of immunogenetic disparity between tumor and recipient governed the intensity and specificity of the host's immune response to the intraocular neoplasm. Our histopathologic studies confirm this conclusion. BALB/c mice, which are H-2 syngeneic with P815 cells, develop progressively growing tumors around which no evidence of host immune or inflammatory response can be found. P815 cells confront A/J mice with a single class I MHC disparity; early intraocular tumor growth is vigorous in this strain, and when the tumor rejection takes place, it is followed by marked fibrovascular scar tissue formation which destroys intraocular structures, resulting in atrophia bulbi. C57BL/6 mice recognize immunologically three categories of allogeneic class I antigens on P815 cells. In these hosts, early tumor growth within the anterior chamber is feeble and rejection is attended by only minimal inflammation; as a consequence, scar formation is trivial and the eye remains anatomically intact. Based on certain histopathologic features, the authors suggest that two distinctly different immune effector mechanisms are involved in intraocular tumor rejection in A/J and C57BL/6 hosts. One immune rejection process results in extensive innocent bystander destruction of normal host tissues (A/J mice) while the other immune mechanism is more precise and does not damage host ocular structures (C57BL/6 mice).