CULTURED MOUSE KERATINOCYTE ALLOGRAFTS PRIME FOR ACCELERATED 2ND SET REJECTION AND ENHANCED CYTOTOXIC LYMPHOCYTE-RESPONSE

Citation
Ba. Cairns et al., CULTURED MOUSE KERATINOCYTE ALLOGRAFTS PRIME FOR ACCELERATED 2ND SET REJECTION AND ENHANCED CYTOTOXIC LYMPHOCYTE-RESPONSE, Transplantation, 58(1), 1994, pp. 67-72
Citations number
31
Categorie Soggetti
Immunology,Surgery
Journal title
ISSN journal
00411337
Volume
58
Issue
1
Year of publication
1994
Pages
67 - 72
Database
ISI
SICI code
0041-1337(1994)58:1<67:CMKAPF>2.0.ZU;2-E
Abstract
It has been reported that cultured keratinocyte (CK) allografts are no t rejected in mice, unlike in other species. Several reports have sugg ested that mouse CK allografts are incapable of stimulating a primary alloresponse, including sensitization of recipients to alloantigens. I n this study, we investigated the immunogenicity of mouse CK allograft s in vivo by determining whether CK allografts primed for a second set rejection response. First, we grafted mice with either CK allografts, CK autografts, full-thickness (FT) allografts, or no graft at all. We then regrafted mice 4 weeks later with a tail skin allograft. Mice gr afted with CK allografts rejected second allografts as rapidly and as vigorously as mice grafted with FT flank allografts. Next, we tested w hether CK allograft primed recipients for enhanced CTL responses. We f ound that mice grafted with CK allografts generated a significantly en hanced CTL alloreactive response after in vitro stimulation. The respo nse was similar to that of mice grafted with FT skin allografts. With evidence that CK allografts primed, we biopsied wounds immediately aft er CK allografting and, using Western immunoblotting, found that CK al lografts had substantial expression of MHC class II antigens in vivo. We conclude from the results of our studies that mouse CK allografts u nequivocally prime recipients to alloantigens in vivo and suggest that a possible mechanism for alloantigen priming may be CK allograft expr ession of MHC class II antigens.