102 R. E. BILLINGHAM AND WILLYS K. SILVERS 



occasioned by grafting, get into the hosts' vessels or tissues, and 

 elicit an effective level of sensitization. The finding that relatively 

 small numbers of homologous leucocytes can sensitize hosts in 

 respect of established pouch skin homografts adds some plausibihty 

 to this hypothesis. Hov^ever, no evidence v^as forthcoming in its 

 favour. The fate of cheek pouch skin homografts prepared from 

 thoroughly exsanguinated donors v^as found not to differ from 

 that of similar homografts from unbled donors. 



(2) When trimming the raw surfaces of pouch skin grafts to 

 facilitate their prompt healing, lesions may sometimes be inflicted 

 in the postulated connective tissue barrier, so that the host does 

 get stimulated antigenically, with consequent destruction of the 

 graft. Although it cannot be refuted, this explanation, like the 

 barrier hypothesis itself, is not without serious shortcomings. For 

 example, if pouch skin homografts are deliberately transplanted 

 as very "open fits", so that their margins are separated from host 

 skin by an annulus of raw bed several millimetres wide, the granu- 

 lation tissue that builds up becomes resurfaced, in part, by out- 

 growth of homologous cheek pouch epithelium which is in 

 direct contact with host mesenchymal tissue. Although resurfaced 

 granulation tissue is a transient structure, more or less obliterated 

 by wound contracture, one might reasonably have anticipated, on 

 the barrier hypothesis, that the host would have been sensitized 

 since homografts of pure epidermis prepared from ordinary 

 skin are antigenically effective (Billingham and Sparrow, 1954). 

 However, the long-term survival of some pouch skin homografts 

 of this type indicates that this does not always occur. 



Influence of cortisone on fate of pouch skin homografts 



Since the homograft reaction in hamsters is very susceptible to 

 the action of cortisone (Billingham and Hildemann, 1958), which 

 according to Scothorne (1956) acts principally by reducing the 

 power of skin homografts to elicit an immune response, through 



