Induction and Regulation of Contact Hypersensitivity in Syrian Hamsters

Abstract

Syrian hamsters were introduced into experimental biology more than 50 years ago when it was found that they were particularly useful for the study of certain parasitic diseases (1). Within a relatively short period of time, their usefulness as experimental subjects was extended into several seemingly unrelated fields. They came to be used extensively for the study of experimental neoplasms (2), virus infections (3), and transplantation immunology (4). After the first 20 years of experience, the hamster came to be regarded as a relatively unique experimental subject because of certain putative aberrations: 1. hamsters reject skin allografts poorly or not at all (4); 2. hamsters are unusually susceptible to induction of tumors with a variety of oncogenic agents (2); 3. hamsters are highly susceptible to infection with viruses from many different species (3). Over the last two decades immunologists have learned that rejection of allografts, resistance to viral infection, and resistance to tumor induction are properties of the immune response that are presided over by the thymus and its cellular progeny. Because of the paramount role played by the thymus-dependent system in these various immune reactivities, it seemed reasonable to question the nature and extent of thymic function in the Syrian hamster. Surprisingly little is known about the T-cell system in this species. It was discovered more than 15 years ago that the ontogenetic maturation of the thymus as studied histologically is delayed (5). Evidence in support of this idea includes the facts that: 1. induction of neonatal transplantation tolerance can be achieved in hamsters up to a week following birth (4); 2. seeding of peripheral lymphoid organs with lymphocytes labeled intrathymically is delayed following birth compared to mice and rats (6); and 3. thymectomy performed as late as four weeks after birth results in a progressive wasting syndrome in hamsters resembling that following neonatal thymectomy in mice and rats (5,7). More recently, it has been found that hamsters fail to regulate certain alloimmune reactions thought to be governed by functional subsets of T lymphocytes in mice and other species. For example, hamsters fail to suppress graft-versus-host reactions in vivo following specific alloimmunization (8), and they do not develop suppressor cells in mixed lymphocyte cultures designed to delineate a putative allogeneic T-cell suppressor (9). In response to alloimmunization in vivo or in vitro, hamster lymphoid cells fail to assume significant cytotoxic activity as measured in vitro (10). Moreover, there is evidence that hamsters fail to develop cytotoxic T cells in response to acute virus infection (11).