Abstract
The classical inbred strains of Syrian hamsters, MHA, LSH, CB, and PD4, display strong cellular alloimmune reactions as indicated by acute skin graft rejection (1,2), strong mixed lymphocyte reactivity (1), and potent graft-vs-host reactivity (1,3); they are unable, however, to develop detectable alloantibody responses to strong histocompatibility determinants (4–6). This quality of the immune response to transplantation alloantigens appears to be unique in hamsters, since in all other species, strong transplantation alloantigens elicit potent alloantibody responses (7–12). Several hypotheses have been advanced to explain this paradox: 1. domesticated Syrian hamsters display a rather limited genetic polymorphism, i.e., because of their derivation from a restricted gene pool, they may differ only at several minor histocompatibility loci but not at a major histocompatibility complex (MHC) equivalent; 2. hamster B cells fail to recognize or respond to MHC-like determinants; 3. Syrian hamsters as a species display little or no polymorphism at their MHC equivalent, Hm-1.
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