Walker 256 tumor MHC class I expression during the shift from A variant to the immunogenic AR variant.
Novel tumor cell variants can be obtained by serially passaging tumor cells in different media and/or environments. Serial intraperitoneal (ip) passages of the Walker 256 tumor A variant was followed for studying the generation of its regressive AR variant. MHC class I molecule expression was assessed since variations in this molecule would explain changes in tumor cell immunogenicity and therefore, the shift from progressive A variant to the regressive AR variant. Within 25 ip passages all serial repetitions shifted from A to AR variant, which was characterized by a significant increase in red blood cell (RBC) osmotic fragility with marked spleen hypertrophy in the host. In one serial repetition AR tumor cells were rejected (ip passage number 36) and immunity against the AR and A variants was conferred. Flow cytometry analysis showed a significant increase in the number MHC class I positive cells in AR variant (n = 15, 14.21 +/- 1.32) compared with A variant (n = 10, 9.10 +/- 1.22). These data provide evidence that the generation of the AR variant could result from factors present in the ip environment leading to an increase in the number of Walker 256 MHC class I positive tumor cells, probably due to immune selection of MHC class I negative tumor cells.
Schanoski
Alessandra Soares
AS
Laboratório de Pesquisas Bioquímicas, Centro de Assistência Integral à Saúde da Mulher, Universidade Estadual de Campinas, P O Box 6081, CEP 13083-970, Campinas, SP, Brazil.
Cavalcanti
Tereza Cristina
TC
Campos
Cláudia Barbosa Ladeira
CB
Viera-Matos
Ana Neuza
AN
Rettori
Ovídio
O
Guimarães
Fernando
F
D000818:Animals; D002279:Carcinoma 256, Walker / Q000276:immunology*; D014644:Genetic Variation; D015395:Histocompatibility Antigens Class I / Q000378:metabolism*; D008297:Male; D051381:Rats; D017208:Rats, Wistar
D015395:Histocompatibility Antigens Class I