Induction of anterior chamber-associated immune deviation requires an intact, functional spleen

When allogeneic P815 mastocytoma cells (derived from DBA/2 mice) are injected into the anterior chamber of the eyes of BALB/c mice, they take advantage of the immunologic privilege within this site (1). The tumor cells proliferate relentlessly until the injected eye is destroyed and/or the tumor invades the cranial vault by direct extension and kills the host. We have reported previously that the intracameral (IC)¹ success of P815 is accompanied by a profound alteration in the capacity of tumor-bearing BALB/c mice to respond to minor histocompatibility antigens of DBA/2 tissues. BALB/c mice with progressively growing intraocular P815 tumors are unable to reject to minor orthotopically grafted DBA/2 skin, although the animals retain the capacity to reject third party C57BL/6 skin grafts (2). The alteration in immune responsiveness in these animals resembled F₁ lymphocyte-induced immune deviation described in rats by Kaplan and Streilein (3). To identify the unique systemic immune responses of animals bearing allogeneic tissues in their anterior chambers we propose the generic term, anterior chamber-associated immune deviation (ACAID). We have described three separate manifestations of ACAID in BALB/c mice innoculated IC with P815 cells: (a) progressive growth of the tumor locally; (b) transient, significant growth of tumors at subcutaneous (SC) sites where P815 cells have also been injected; and (c) prolonged (and usually indefinite) acceptance of DBA/2 skin grafts placed on their thoracic cages. Our previous studies of the ACAID phenomenon in rats produced evidence that alloantigens presented via the anterior chamber evoke both destructive and protective host immune responses (4). The data further suggested that regulation of the relative participation of protective/destructive host forces was focused within the intact spleen (5). In this paper, we describe the results of experiments designed to examine a putative splenic role in ACAID as it is elicited in BALB/c mice by the IC inoculation of P815 mastocytoma cells.